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high permeability pulmonary edema contributes significantly to the development of the disease and represents a potential target for early preventative therapy&#46; Pulmonary edema is determined by the Starling relationship&#44; which predicts the net flow of liquid across a membrane&#46; In high permeability pulmonary edema&#44; the most common mechanism for a rise in the transcapillary filtration of fluids is an increase in capillary permeability&#46; However&#44; experimental studies demonstrated that&#44; at a given increase in capillarity permeability&#44; a modest change in pulmonary vascular pressure greatly modifies the quantity of pulmonary edema&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">9</span></a> This is probably one of the reasons why a strategy of restricting the administration of fluids has demonstrated to be useful in ARDS for decreasing pulmonary edema and improving lung function&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">10</span></a> However&#44; whether this strategy restraining fluid administration may also be useful in preventing the development of ARDS is not well known&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">We hypothesized that a preemptive hemodynamic intervention by restricting the administration of fluids&#44; right at the very start of lung injury&#44; would be successful in reducing the formation and the progression of pulmonary edema&#44; decreasing the severity of the resulting respiratory failure&#46; We refer to this strategy as the early protective lung strategy &#40;EPLS&#41; and compare it against another strategy to maintain hemodynamic stability&#44; which we call the early protective hemodynamic strategy &#40;EPHS&#41;&#46; In this study&#44; we applied from the very inception of the injury and pulmonary inflammation in a rabbit model of lung injury with the involvement of the cardio circulatory function&#44; induced by continuous intravenous administration of oleic acid &#40;OA&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0255"><span class="elsevierStyleSup">11&#8211;13</span></a></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Materials and methods</span><p id="par0020" class="elsevierStylePara elsevierViewall">Sixteen New Zealand rabbits &#40;weight 2&#46;8<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>0&#46;2<span class="elsevierStyleHsp" style=""></span>kg&#41;&#44; supplied by the Reproduction Laboratory of the University of Cadiz&#44; were maintained in individual cages on a 12-hour light&#47;dark cycle with free access to food and water until the time of the experimental procedures&#46; All of the procedures and protocols in this investigation were reviewed and approved by the Ethical Committee for Animal Experimentation of the School of Medicine of the University of Cadiz&#46; The animal care and use procedures conformed to European Ethical Standards <span class="elsevierStyleItalic">&#40;European Union Directive 86&#47;609 and Spanish Royal Decree 1201&#47;2005&#41;</span> for the care and use of laboratory animals for experimental research&#46;</p><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Animal preparation and instrumentation</span><p id="par0025" class="elsevierStylePara elsevierViewall">The animals were anesthetized with xylazine &#40;10<span class="elsevierStyleHsp" style=""></span>mg&#47;kg intramuscularly&#41; and Ketamine &#40;40<span class="elsevierStyleHsp" style=""></span>mg&#47;kg intramuscularly&#41;&#46; The animals were tracheotomized&#44; intubated&#44; and mechanically ventilated with volume-controlled ventilation &#40;Siemens Servo 900C ventilator&#44; Siemens-Elema AB&#44; Solna&#44; Sweden&#41; at a tidal volume of 8<span class="elsevierStyleHsp" style=""></span>ml&#47;kg&#44; a positive end expiratory pressure &#40;PEEP&#41; of 3<span class="elsevierStyleHsp" style=""></span>cmH<span class="elsevierStyleInf">2</span>O&#44; an inspiration to expiration ratio of 1&#58;2&#44; a respiratory rate of 35&#47;minute&#44; and an inspired oxygen fraction of 0&#46;6&#46; The anesthesia was maintained with a continuous intravenous infusion of ketamine &#40;20<span class="elsevierStyleHsp" style=""></span>mg<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#41; and xylazine &#40;6<span class="elsevierStyleHsp" style=""></span>mg<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#41;&#46; A muscular blockade was maintained with a rocuronium bromide infusion &#40;0&#46;1<span class="elsevierStyleHsp" style=""></span>mg<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#41;&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Respiratory monitoring</span><p id="par0030" class="elsevierStylePara elsevierViewall">Continuous non-invasive measurements of flow&#44; pressure&#44; and volume in the animal&#39;s airway were measured using a calibrated CO<span class="elsevierStyleInf">2</span>SMO Plus&#33; monitor &#40;Respironics Novametrix Medical System INC&#44; Wallingford&#44; CT&#44; USA&#41; with a neonatal flow sensor connected directly to the animal&#39;s tracheal tube&#46;<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">14</span></a> Dynamic compliance &#40;<span class="elsevierStyleItalic">C</span><span class="elsevierStyleInf">dyn</span>&#41;&#44; inspiratory and expiratory airway resistance &#40;<span class="elsevierStyleItalic">R</span><span class="elsevierStyleInf">awi</span>&#44; <span class="elsevierStyleItalic">R</span><span class="elsevierStyleInf">awe</span>&#41;&#44; dynamic intrinsic PEEP &#40;auto-PEEP&#41;&#44; and total inspiratory work of breathing &#40;WOB&#41; were continuously computed by least squares fitting of the flow&#44; volume&#44; and pressure raw waveform data to a simple model&#46;<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">15</span></a> Data were downloaded via a RS232 connection to a laptop computer for collection and posterior review using data acquisition software &#40;Analysis&#43;&#44; Novametrix Medical System INC&#44; Wallingford&#44; CT&#44; USA&#41;&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Hemodynamic monitoring</span><p id="par0035" class="elsevierStylePara elsevierViewall">Commercially available Doppler equipment &#40;Cardio QPTM&#44; Deltex Medical TM&#44; Chichester&#44; UK&#41; with a 4<span class="elsevierStyleHsp" style=""></span>MHz flexible pediatric transesophageal probe &#40;KDP n-Kinder Doppler Probe<span class="elsevierStyleSup">&#174;</span>&#41; was used for the studies&#46;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">16</span></a> The probe was introduced into the rabbit at mid-esophagus until the aortic blood flow signals were best identified&#46; The optimal position of the probe was suggested by an audible&#44; maximal pitch and a sharply defined velocity waveform with minimal spectral dispersion&#46; Consecutive transesophageal Doppler measurements for 60<span class="elsevierStyleHsp" style=""></span>s at the beginning&#44; at 1<span class="elsevierStyleHsp" style=""></span>h&#44; and at 2<span class="elsevierStyleHsp" style=""></span>h &#40;end of experiment&#41; were completed and averaged to calculate the cardiac index &#40;CI&#41; &#40;cardiac output divided by the weight&#41;&#44; the corrected flow time &#40;cFT&#41; &#40;length of time of systolic blood flow adjusted for heart rate&#44; &#91;i&#46;e&#46;&#44; divided by the square root of the heart cycle time&#93;&#41;&#44; the peak velocity &#40;PV&#41; &#40;maximal velocity during systole&#41;&#44; and the mean acceleration &#40;MA&#41; &#40;PV divided by the acceleration time during systole&#41; of the descending aorta velocity waveform&#46;<a class="elsevierStyleCrossRefs" href="#bib0285"><span class="elsevierStyleSup">17&#8211;19</span></a> The arterial pressure was measured by an indwelling femoral artery catheter connected to a pressure transducer &#40;TruWave<span class="elsevierStyleSup">&#174;</span>&#44; Edwards Lifesciences LLC&#44; Irvine&#44; CA&#44; USA&#41;&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0125">Experimental protocol</span><p id="par0040" class="elsevierStylePara elsevierViewall">Immediately after the baseline measurement of hemodynamic and lung mechanics&#44; the animals were randomly assigned to the EPLS group &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>8&#41; or the EPHS group &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>8&#41;&#44; and the lung injury was induced by continuous intravenous infusion of OA &#40;0&#46;133<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> for 2<span class="elsevierStyleHsp" style=""></span>h&#41; via the central venous catheter&#46;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">11</span></a> During this period&#44; the EPLS group received 15<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> of Ringer Lactate&#44; and the EPHS group received 30<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#46; Once 2<span class="elsevierStyleHsp" style=""></span>h elapsed&#44; all of the rabbits were killed by an injection of a lethal dose of chloride potassium&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">At the end of the experiment&#44; the thorax was opened&#44; and the lungs were removed en bloc&#46; The right lung was weighed and then dried in a microwave oven at a power of 150<span class="elsevierStyleHsp" style=""></span>W for 60<span class="elsevierStyleHsp" style=""></span>min&#46;<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">20</span></a> The ratio of wet weight to dry weight &#40;WW&#47;DW&#41; of the right lung was calculated to assess tissue edema&#46; The left lung was excised and immersed in 10&#37; formaldehyde for at least 72<span class="elsevierStyleHsp" style=""></span>h&#46; Tissue samples were dehydrated with graded alcohol&#44; embedded in paraffin&#44; and cut in a series of 4<span class="elsevierStyleHsp" style=""></span>&#956;m-thick slices that were stained with hematoxylin and eosin&#46; A pathologist &#40;JRC&#41; then evaluated these tissue sections in a blinded fashion using the following scoring system to grade the degree of lung injury&#58; 0 &#40;no damage&#41; to 3 &#40;maximal damage&#41;&#46; These score were according to the combined assessments of alveolar congestion&#44; alveolar hemorrhage and edema&#44; infiltration&#47;aggregation of the neutrophils in the airspace or vessel wall&#44; the thickness of the alveolar wall&#44; bronchiole epithelial desquamation&#44; and hyaline membrane formation</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0130">Statistical analysis</span><p id="par0050" class="elsevierStylePara elsevierViewall">Unless otherwise indicated&#44; the results are presented as mean<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>SD&#46; Data were tested for normal distribution with the Agostino-Pearson test&#46; We used a two-way analysis of variance for repeated measures to determine the statistical significance of group differences in the respiratory parameters and the Doppler transesophageal measurements at different time points&#46; When statistical significance was indicated&#44; it was further examined by a post hoc analysis &#40;Student&#8211;Newman&#8211;Keuls test&#41;&#46; A Student&#39;s unpaired <span class="elsevierStyleItalic">t</span>-test was used for single-time point observation&#46; Results from the histological studies are expressed as median and range&#44; and the statistical analysis was performed using the Mann Whitney <span class="elsevierStyleItalic">U</span>-test&#46; Data were analyzed by using MedCalc Statistical Software &#40;version 9&#46;5&#46;2&#46;0&#59; MedCalc Software bvba&#44; Ostend&#44; Belgium&#41;&#46; Statistical significance was assumed at a probability &#60;0&#46;05&#46;</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0135">Results</span><p id="par0055" class="elsevierStylePara elsevierViewall">In 16 rabbits randomly allotted to each of the two groups &#40;EPLS and EPHS&#41;&#44; we found that at the beginning of the experiment&#44; each group had similar baseline characteristics for any of the hemodynamic and respiratory variables measured &#40;<a class="elsevierStyleCrossRefs" href="#tbl0005">Tables 1 and 2</a>&#41;&#46; The total fluid intake &#40;i&#46;e&#46;&#44; sedation&#44; oleic preparation&#44; and fluid therapy&#41; was 19&#46;8<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> in the EPLS group and 36&#46;2<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> in the EPHS group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;001&#41;&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0140">Hemodynamic changes</span><p id="par0060" class="elsevierStylePara elsevierViewall">As shown in <a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#44; both strategies shown different hemodynamic effects&#46; Compared with the baseline&#44; there was a decrease in the CI that reached statistical significance in the animals in the EPLS group&#59; however in the animals in the EPHS group&#44; the CI remained unchanged throughout the experiment&#46; Heart rate decreased significantly in the animals in the EPHS group&#44; and by the end of the experiment&#44; the cFT was significantly higher in the EPHS group &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0145">Respiratory changes</span><p id="par0065" class="elsevierStylePara elsevierViewall">As shown in <a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#44; the two strategies had different effects on respiratory mechanics&#46; Compared to the baseline&#44; at 1 and 2<span class="elsevierStyleHsp" style=""></span>h &#40;end of experiment&#41;&#44; the <span class="elsevierStyleItalic">C</span><span class="elsevierStyleInf">dyn</span> had decreased significantly only in animals in the EPHS group&#46; Other measurements of respiratory mechanics&#44; <span class="elsevierStyleItalic">R</span><span class="elsevierStyleInf">awi</span>&#44; <span class="elsevierStyleItalic">R</span><span class="elsevierStyleInf">awe</span> and WOB&#44; increased more in the EPHS group&#44; although without statistical significance&#46; No animals in either group showed auto-PEEP&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0150">Lung edema and descriptive histology</span><p id="par0070" class="elsevierStylePara elsevierViewall">Pulmonary edema estimation by calculating the WW&#47;DW ratio was increased in the two groups&#44; but it was higher in the EPHS group than in the EPLS group &#40;6&#46;8<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>0&#46;8<span class="elsevierStyleHsp" style=""></span>g in the EPHS group and 5&#46;8<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>0&#46;8<span class="elsevierStyleHsp" style=""></span>g in the EPLS&#44; <span class="elsevierStyleItalic">p</span>&#58; 0&#46;02&#59; normal value in our laboratory &#8764;5<span class="elsevierStyleHsp" style=""></span>g&#41;&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">In all of the animals&#44; the lungs exhibited gross damage&#44; including edema with petechial hemorrhages on the surface&#59; however&#44; the lungs of the animals in the EPHS group exhibited more intense damage&#44; especially hemorrhages &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46; The histological findings&#44; including alveolar congestion&#44; interstitial and alveolar infiltration&#47;aggregation of neutrophils&#44; alveolar membrane focal thickening&#44; alveolar edema or hemorrhage&#44; bronchiole epithelial desquamation&#44; and hyaline membranes were present in similar degrees in both groups &#40;lung injury score 8&#46;5<a class="elsevierStyleCrossRefs" href="#bib0235"><span class="elsevierStyleSup">7&#8211;11</span></a> in the EPHS group and 8&#46;5<a class="elsevierStyleCrossRefs" href="#bib0230"><span class="elsevierStyleSup">6&#8211;9</span></a> in the EPLS group&#59; <span class="elsevierStyleItalic">p</span>&#58; 0&#46;4&#41;&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia></span></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0155">Discussion</span><p id="par0080" class="elsevierStylePara elsevierViewall">The main finding of this experimental study is that a preemptive hemodynamic intervention by restricting the administration of fluids significantly slowed the progression of pulmonary edema and the decreased pulmonary compliance in OA-induced acute lung injury&#46; When fluids were administered more liberally to focus on ensuring the hemodynamic stability&#44; pulmonary edema progression was higher and <span class="elsevierStyleItalic">C</span><span class="elsevierStyleInf">dyn</span> decreased more than when fluids were infused in smaller quantities that were insufficient to prevent hemodynamic deterioration&#46; Therefore&#44; the EPHS proved useful to maintain hemodynamic stability&#44; but it was detrimental to the progression of pulmonary edema&#59; conversely&#44; the EPLS was successful in reducing the progression of pulmonary edema&#44; but it was not effective in preventing hemodynamic deterioration&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">ARDS is a catastrophic form of lung injury characterized in more than half of patients by diffuse alveolar damage with severe inflammation and high permeability protein-rich edema in the lungs&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">8</span></a> This syndrome produces results that are notoriously difficult to treat once the diagnosis is made and has an associated mortality approaching 40&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">21</span></a> Recent studies suggest that the development of lung damage represents a progression of pathology in the lung between the time of insult and the time at which ARDS criteria are met&#46;<a class="elsevierStyleCrossRefs" href="#bib0310"><span class="elsevierStyleSup">22&#44;23</span></a> During this period of time&#44; referred to by some as the silent phase&#44;<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">24</span></a> further attacks or impacts &#40;i&#46;e&#46;&#44; second hits&#41; frequently occur&#46; These attacks contribute to the gradual progression from initial mild-moderate lung injury to clinical ARDS&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">4&#8211;7</span></a> Most of the time&#44; the second hits are iatrogenic insults&#44; including transfusions&#44; mechanical ventilations with high tidal volumes&#44; delayed treatments of shock and infection&#44; and the inappropriate administration of fluids&#46; Because of the second hits favoring the progression from mild to severe lung injury fulfilling the criteria for ARDS with devastating respiratory failure&#44; there are reasons to believe that the prevention of these hits should result in a decrease in the incidence and severity of ARDS&#46;<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">5</span></a> In this regard&#44; we think that our results suggest that fluid administration&#44; even cautiously adjusted to maintain cardiac output&#44; might behave as a second hit influencing the progression of pulmonary edema and favoring the development of ARDS&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">The relationship between the administration of fluids and the development of ARDS was already stated over 40 years ago during periods of war&#46; During these times&#44; it was observed that many patients who had suffered severe trauma were strongly raised with crystalloid solutions and were stabilized in the battle field&#46; Later in the hospital&#44; these patients developed a very severe hypoxemic respiratory failure due to pulmonary edema&#44; which often led to death&#46; This entity&#44; called &#8220;wet lung&#8221;&#44;<a class="elsevierStyleCrossRefs" href="#bib0325"><span class="elsevierStyleSup">25&#44;26</span></a> at autopsy was characterized by histopathological changes similar to those described later in ARDS&#46;<a class="elsevierStyleCrossRefs" href="#bib0335"><span class="elsevierStyleSup">27&#44;28</span></a> In the civil stage&#44; several studies have reported a relationship between a positive fluid balance and the development of ARDS<a class="elsevierStyleCrossRefs" href="#bib0345"><span class="elsevierStyleSup">29&#8211;33</span></a>&#59; however&#44; to date&#44; there is a widespread opinion that it is difficult to establish whether or not this relationship represents a simple association or a cause-and-effect relationship&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">34</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">During the onset of lung injury and the development of diffuse alveolar damage&#44; high permeability pulmonary edema has a central role&#44; acting as a driving force that reduces the airspace available for normal gas exchange and contributes to the disruption of surfactant&#44; which leads to alveolar instability and collapse&#46; Pulmonary edema is determined by the Starling relationship&#44; which predicts the net flow of liquid across a membrane&#46; In acute lung injury&#44; the most common mechanism for a rise in the transcapillary filtration of fluids is an increase in capillary permeability&#46;<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">35</span></a> However&#44; experimental studies demonstrated that&#44; at a given increase in capillarity permeability&#44; a modest change in pulmonary vascular pressure greatly modifies the quantity of pulmonary edema&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">9</span></a> That is probably why a strategy of restricting the administration of fluids has demonstrated to be useful in acute lung injury for decreasing pulmonary edema and improving lung function&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">10</span></a> The novelty of our study is that&#44; when this strategy of restricting the administration of fluids was used at the very inception of the injury and pulmonary inflammation&#44; there was less pulmonary edema and less affectation of the respiratory mechanics&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">On the other hand&#44; the strategy based on restricting the fluid administration&#44; inadequately maintained cardiac output&#46; The main hemodynamic consequences of OA infusion are a sharp increase in pulmonary vascular resistance with the elevation of pulmonary artery pressure and a significant decline in cardiac output and heart rate&#46;<a class="elsevierStyleCrossRef" href="#bib0380"><span class="elsevierStyleSup">36</span></a> Moreover&#44; depending of the doses and the velocity of OA administration&#44; systemic vascular collapse can develop&#46; To reverse the cardiac consequences of OA administration&#44; energetic fluid infusion and&#47;or inotropic drugs are frequently used&#46; For results in the benefits&#44; the fluid administration must increase the heart preload&#44; thereby increasing the systolic volume and the cardiac output&#46; In addition to the cardiac output&#44; transesophageal Doppler measurements include the cFT&#44; a parameter that&#44; although is influenced by the afterload&#44; has been proposed as a value of the preload&#46;<a class="elsevierStyleCrossRefs" href="#bib0290"><span class="elsevierStyleSup">18&#44;37</span></a> By the end of experiment&#44; the cFT was higher in the EPHS group&#44; and therefore&#44; we believe that the animals in the EPHS group maintained cardiac output&#44; at least during the second hour of the experiment&#44; mainly by increasing the cardiac preload&#46; However&#44; the importance of maintaining the cardiac output during ARDS development is not well known&#46; Although adequate cardiac output is necessary to ensure enough oxygen delivery&#44; high cardiac output can be detrimental for lung injury enhancing transcapillary filtration and pulmonary edema&#46;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">38</span></a> Therefore&#44; it is possible that in our experiment&#44; a slight decrease in the cardiac output in the animals in the EPLS group was useful to protect the lungs&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">In addition to the experimental nature of this study&#44; there are some limitations to our study&#46; First&#44; the lung injury model we used&#46; Although OA administered to animals increases pulmonary vascular permeability and produces a condition that pathophysiologically resembles acute lung injury in humans&#44;<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">13</span></a> the severity or extensiveness of the injury depends on the doses and the direction of the OA administration&#58; a simple bolus&#44; repeated injections&#44; or a continuous infusion&#46; We chose a model by a slow and steady infusion of OA for 2<span class="elsevierStyleHsp" style=""></span>h<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">11</span></a> that provides a better hemodynamic tolerance and allows for the monitoring of hemodynamic and respiratory changes in detail&#46; However&#44; when the OA is administered in this way&#44; lung damage may progress for at least 6<span class="elsevierStyleHsp" style=""></span>h&#46;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">11</span></a> Therefore&#44; it is very likely that the short duration of our study prevented the full development of lung injury in both of the groups&#46; Another important aspect of the study is the way in which the fluids were administered&#46; For the EPHS group&#44; we selected a set amount of fluid to keep CI based on previous preliminary observations we made in our laboratory&#46; However&#44; it is possible that the animals in the EPHS group received an excessive and inadequate amount of fluids&#44; and a component of overhydration was present&#46; Obviously the inclusion of a sham group could have helped to clarify this issue&#46; With respect to the measurement of cardiac output by oesophageal Doppler there is little experience about precision in small animals&#44;<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">39</span></a> but we believe that a previous analysis published by our own group<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">40</span></a> strongly supports the accuracy of the reported differences in CI between the two groups&#46; Finally&#44; although we graded the histopathologic findings using a scoring system&#44; we did not perform an extensive study&#46; The fact that there was more macroscopic involvement in the lungs of the EPHS group &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#44; raises the question that the histological damage was also more extensive in this group&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">In conclusion&#44; the results of our study entrench a cause-and-effect relationship between fluids and the development of pulmonary edema at the beginning of acute lung injury with diffuse alveolar damage and demonstrate that&#44; at the very inception of the injury and the pulmonary inflammation&#44; an early strategy of restricting the infusion of fluids is associated with a reduction in the progression of pulmonary edema and the deterioration of lung mechanics&#46; Thus&#44; we believe that in a clinical setting with patients at risk of developing ARDS a strategy of restricting the administration of fluids should be investigated&#46;</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0160">Funding</span><p id="par0115" class="elsevierStylePara elsevierViewall">This study did not receive any funding after being rejected twice by the Ministry of Health of the Government of Andalusia in 2008 calls &#40;PI-0174&#41; and 2009 &#40;PI-0264&#41;&#46;</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0165">Conflict of interests</span><p id="par0120" class="elsevierStylePara elsevierViewall">Anselmo Gil Cano has received Honoraria from Edwards Lifesciences&#46; Manuel Ignacio Monge Garc&#237;a was consultant for Edwards Lifesciences and received travel expenses from Deltex&#46; Manuel Gracia Romero&#44; Pedro Guijo Gonz&#225;lez and Jos&#233; Ruiz Campos have no conflict of interest to declare&#46;</p></span></span>"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Objective</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">A study is made of the influence of preemptive hemodynamic intervention restricting fluid administration upon the development of oleic acid-induced lung injury&#46;</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Design</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">A randomized in vivo study in rabbits was carried out&#46;</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Setting</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">University research laboratory&#46;</p></span> <span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Subjects</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Sixteen anesthetized&#44; mechanically ventilated rabbits&#46;</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Variables</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Hemodynamic measurements obtained by transesophageal Doppler signal&#46; Respiratory mechanics computed by a least square fitting method&#46; Lung edema assessed by the ratio of wet weight to dry weight of the right lung&#46; Histological examination of the left lung&#46;</p></span> <span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Interventions</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Animals were randomly assigned to either the early protective lung strategy &#40;EPLS&#41; &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>8&#41; or the early protective hemodynamic strategy &#40;EPHS&#41; &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>8&#41;&#46; In both groups&#44; lung injury was induced by the intravenous infusion of oleic acid &#40;OA&#41; &#40;0&#46;133<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> for 2<span class="elsevierStyleHsp" style=""></span>h&#41;&#46; At the same time&#44; the EPLS group received 15<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> of Ringer lactate solution&#44; while the EPHS group received 30<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#46; Measurements were obtained at baseline and 1 and 2<span class="elsevierStyleHsp" style=""></span>h after starting OA infusion&#46;</p></span> <span id="abst0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Results</span><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">After 2<span class="elsevierStyleHsp" style=""></span>h&#44; the cardiac index decreased in the EPLS group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#44; whereas in the EPHS group it remained unchanged&#46; Lung compliance decreased significantly only in the EPHS group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#46; Lung edema was greater in the EPHS group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#46; Histological damage proved similar in both groups &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;4&#41;&#46;</p></span> <span id="abst0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conclusions</span><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">In this experimental model of early lung injury&#44; lung edema progression was attenuated by preemptively restricting the administration of fluids&#46;</p></span>"
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        "resumen" => "<span id="abst0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Objetivo</span><p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Conocer c&#243;mo influye una intervenci&#243;n hemodin&#225;mica preventiva basada en la restricci&#243;n de fluidos sobre el desarrollo de la lesi&#243;n pulmonar inducida por la administraci&#243;n de &#225;cido oleico&#46;</p></span> <span id="abst0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Dise&#241;o</span><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">Estudio aleatorizado en animales vivos&#46;</p></span> <span id="abst0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Lugar</span><p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Laboratorio universitario de investigaci&#243;n experimental&#46;</p></span> <span id="abst0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Variables</span><p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Mec&#225;nica respiratoria &#40;m&#233;todo de los m&#237;nimos cuadrados&#41;&#44; medidas hemodin&#225;micas &#40;doppler esof&#225;gico&#41;&#44; estimaci&#243;n del edema pulmonar &#40;relaci&#243;n peso h&#250;medo&#47;seco del pulm&#243;n derecho&#41; y da&#241;o histol&#243;gico del pulm&#243;n izquierdo&#46;</p></span> <span id="abst0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Intervenciones</span><p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Ocho animales fueron asignados a un grupo con una estrategia protectora pulmonar &#40;EPP&#41;&#44; y otros 8 a otro grupo con una estrategia protectora hemodin&#225;mica &#40;EPH&#41;&#46; En ambos grupos la lesi&#243;n pulmonar se desencaden&#243; mediante la administraci&#243;n intravenosa de &#225;cido oleico &#40;0&#44;133<span class="elsevierStyleHsp" style=""></span>mL&#47;kg<span class="elsevierStyleSup">&#8722;1</span>&#47;h<span class="elsevierStyleSup">&#8722;1</span> durante 2<span class="elsevierStyleHsp" style=""></span>h&#41;&#44; recibiendo simult&#225;neamente los animales del grupo EPP 15<span class="elsevierStyleHsp" style=""></span>mL&#47;kg<span class="elsevierStyleSup">&#8722;1</span>&#47;h<span class="elsevierStyleSup">&#8722;1</span> de Ringer Lactato y los del grupo EPH 30<span class="elsevierStyleHsp" style=""></span>mL<span class="elsevierStyleHsp" style=""></span>Kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#46; Se obtuvieron medidas basales&#44; a la hora y a las 2<span class="elsevierStyleHsp" style=""></span>h&#46;</p></span> <span id="abst0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Resultados</span><p id="spar0070" class="elsevierStyleSimplePara elsevierViewall">Transcurridas las 2<span class="elsevierStyleHsp" style=""></span>h de experimento el &#237;ndice cardiaco permaneci&#243; estable en el grupo EPH&#44; pero disminuy&#243; en el grupo EPP &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#46; Por el contrario&#44; la distensibilidad pulmonar disminuy&#243; significativamente solo en el grupo EPH &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#44; en el cual el edema pulmonar estimado mediante la relaci&#243;n peso h&#250;medo&#47;seco del pulm&#243;n derecho fue mayor &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#46; El da&#241;o histol&#243;gico fue similar en ambos grupos &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;4&#41;&#46;</p></span> <span id="abst0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Conclusiones</span><p id="spar0075" class="elsevierStyleSimplePara elsevierViewall">En este modelo experimental de lesi&#243;n pulmonar aguda en fase inicial&#44; la formaci&#243;n del edema pulmonar fue atenuada por la restricci&#243;n preventiva en la administraci&#243;n de fluidos&#46;</p></span>"
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        0 => array:2 [
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                            1 => "I&#46; Martin-Loeches"
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                      "autores" => array:1 [
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                            0 => "M&#46; Yilmaz"
                            1 => "M&#46;T&#46; Keegan"
                            2 => "R&#46; Iscimen"
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                            "web" => "Medline"
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Original
Preemptive hemodynamic intervention restricting the administration of fluids attenuates lung edema progression in oleic acid-induced lung injury
La restricción preventiva en la administración de fluidos disminuye la formación del edema en la lesión pulmonar inducida por ácido oleico
A. Gil Canoa,
Corresponding author
anselgil@gmail.com

Corresponding author.
, M. Gracia Romeroa, M.I. Monge Garcíaa, P. Guijo Gonzáleza, J. Ruiz Camposb
a Laboratorio de Investigación Experimental, Unidad de Gestión Clínica de Medicina Intensiva, Hospital del SAS de Jerez, Jerez de la Frontera, Cádiz, Spain
b Servicio de Anatomía Patológica, Hospital del SAS de Jerez, Jerez de la Frontera, Cádiz, Spain
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further aggravating the initial lung inflammation&#44; and may precipitate the clinical onset of ARDS&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">4&#44;5</span></a> Most commonly&#44; second hits are iatrogenic insults&#44; such as transfusions&#44; mechanical ventilations with high tidal volumes&#44; or the inappropriate administration of fluids&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">4&#8211;6</span></a> The theory of second hits implies that ARDS may have preclinical stages&#44; offering to clinicians an opportunity to intervene earlier before devastating respiratory failure when clinical criteria of ARDS are present&#46; In fact&#44; a recent interdisciplinary intervention aimed at avoiding large tidal volumes and inappropriate transfusions in mechanically ventilated patients was associated with a decreased frequency of new cases of ARDS&#46;<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">7</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">Diffuse alveolar damage with severe inflammation and high permeability protein-rich edema in the lungs represents the most characteristic pathological finding in more than half of patients with ARDS&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">8</span></a> In these patients&#44; high permeability pulmonary edema contributes significantly to the development of the disease and represents a potential target for early preventative therapy&#46; Pulmonary edema is determined by the Starling relationship&#44; which predicts the net flow of liquid across a membrane&#46; In high permeability pulmonary edema&#44; the most common mechanism for a rise in the transcapillary filtration of fluids is an increase in capillary permeability&#46; However&#44; experimental studies demonstrated that&#44; at a given increase in capillarity permeability&#44; a modest change in pulmonary vascular pressure greatly modifies the quantity of pulmonary edema&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">9</span></a> This is probably one of the reasons why a strategy of restricting the administration of fluids has demonstrated to be useful in ARDS for decreasing pulmonary edema and improving lung function&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">10</span></a> However&#44; whether this strategy restraining fluid administration may also be useful in preventing the development of ARDS is not well known&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">We hypothesized that a preemptive hemodynamic intervention by restricting the administration of fluids&#44; right at the very start of lung injury&#44; would be successful in reducing the formation and the progression of pulmonary edema&#44; decreasing the severity of the resulting respiratory failure&#46; We refer to this strategy as the early protective lung strategy &#40;EPLS&#41; and compare it against another strategy to maintain hemodynamic stability&#44; which we call the early protective hemodynamic strategy &#40;EPHS&#41;&#46; In this study&#44; we applied from the very inception of the injury and pulmonary inflammation in a rabbit model of lung injury with the involvement of the cardio circulatory function&#44; induced by continuous intravenous administration of oleic acid &#40;OA&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0255"><span class="elsevierStyleSup">11&#8211;13</span></a></p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Materials and methods</span><p id="par0020" class="elsevierStylePara elsevierViewall">Sixteen New Zealand rabbits &#40;weight 2&#46;8<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>0&#46;2<span class="elsevierStyleHsp" style=""></span>kg&#41;&#44; supplied by the Reproduction Laboratory of the University of Cadiz&#44; were maintained in individual cages on a 12-hour light&#47;dark cycle with free access to food and water until the time of the experimental procedures&#46; All of the procedures and protocols in this investigation were reviewed and approved by the Ethical Committee for Animal Experimentation of the School of Medicine of the University of Cadiz&#46; The animal care and use procedures conformed to European Ethical Standards <span class="elsevierStyleItalic">&#40;European Union Directive 86&#47;609 and Spanish Royal Decree 1201&#47;2005&#41;</span> for the care and use of laboratory animals for experimental research&#46;</p><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Animal preparation and instrumentation</span><p id="par0025" class="elsevierStylePara elsevierViewall">The animals were anesthetized with xylazine &#40;10<span class="elsevierStyleHsp" style=""></span>mg&#47;kg intramuscularly&#41; and Ketamine &#40;40<span class="elsevierStyleHsp" style=""></span>mg&#47;kg intramuscularly&#41;&#46; The animals were tracheotomized&#44; intubated&#44; and mechanically ventilated with volume-controlled ventilation &#40;Siemens Servo 900C ventilator&#44; Siemens-Elema AB&#44; Solna&#44; Sweden&#41; at a tidal volume of 8<span class="elsevierStyleHsp" style=""></span>ml&#47;kg&#44; a positive end expiratory pressure &#40;PEEP&#41; of 3<span class="elsevierStyleHsp" style=""></span>cmH<span class="elsevierStyleInf">2</span>O&#44; an inspiration to expiration ratio of 1&#58;2&#44; a respiratory rate of 35&#47;minute&#44; and an inspired oxygen fraction of 0&#46;6&#46; The anesthesia was maintained with a continuous intravenous infusion of ketamine &#40;20<span class="elsevierStyleHsp" style=""></span>mg<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#41; and xylazine &#40;6<span class="elsevierStyleHsp" style=""></span>mg<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#41;&#46; A muscular blockade was maintained with a rocuronium bromide infusion &#40;0&#46;1<span class="elsevierStyleHsp" style=""></span>mg<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#41;&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Respiratory monitoring</span><p id="par0030" class="elsevierStylePara elsevierViewall">Continuous non-invasive measurements of flow&#44; pressure&#44; and volume in the animal&#39;s airway were measured using a calibrated CO<span class="elsevierStyleInf">2</span>SMO Plus&#33; monitor &#40;Respironics Novametrix Medical System INC&#44; Wallingford&#44; CT&#44; USA&#41; with a neonatal flow sensor connected directly to the animal&#39;s tracheal tube&#46;<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">14</span></a> Dynamic compliance &#40;<span class="elsevierStyleItalic">C</span><span class="elsevierStyleInf">dyn</span>&#41;&#44; inspiratory and expiratory airway resistance &#40;<span class="elsevierStyleItalic">R</span><span class="elsevierStyleInf">awi</span>&#44; <span class="elsevierStyleItalic">R</span><span class="elsevierStyleInf">awe</span>&#41;&#44; dynamic intrinsic PEEP &#40;auto-PEEP&#41;&#44; and total inspiratory work of breathing &#40;WOB&#41; were continuously computed by least squares fitting of the flow&#44; volume&#44; and pressure raw waveform data to a simple model&#46;<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">15</span></a> Data were downloaded via a RS232 connection to a laptop computer for collection and posterior review using data acquisition software &#40;Analysis&#43;&#44; Novametrix Medical System INC&#44; Wallingford&#44; CT&#44; USA&#41;&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Hemodynamic monitoring</span><p id="par0035" class="elsevierStylePara elsevierViewall">Commercially available Doppler equipment &#40;Cardio QPTM&#44; Deltex Medical TM&#44; Chichester&#44; UK&#41; with a 4<span class="elsevierStyleHsp" style=""></span>MHz flexible pediatric transesophageal probe &#40;KDP n-Kinder Doppler Probe<span class="elsevierStyleSup">&#174;</span>&#41; was used for the studies&#46;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">16</span></a> The probe was introduced into the rabbit at mid-esophagus until the aortic blood flow signals were best identified&#46; The optimal position of the probe was suggested by an audible&#44; maximal pitch and a sharply defined velocity waveform with minimal spectral dispersion&#46; Consecutive transesophageal Doppler measurements for 60<span class="elsevierStyleHsp" style=""></span>s at the beginning&#44; at 1<span class="elsevierStyleHsp" style=""></span>h&#44; and at 2<span class="elsevierStyleHsp" style=""></span>h &#40;end of experiment&#41; were completed and averaged to calculate the cardiac index &#40;CI&#41; &#40;cardiac output divided by the weight&#41;&#44; the corrected flow time &#40;cFT&#41; &#40;length of time of systolic blood flow adjusted for heart rate&#44; &#91;i&#46;e&#46;&#44; divided by the square root of the heart cycle time&#93;&#41;&#44; the peak velocity &#40;PV&#41; &#40;maximal velocity during systole&#41;&#44; and the mean acceleration &#40;MA&#41; &#40;PV divided by the acceleration time during systole&#41; of the descending aorta velocity waveform&#46;<a class="elsevierStyleCrossRefs" href="#bib0285"><span class="elsevierStyleSup">17&#8211;19</span></a> The arterial pressure was measured by an indwelling femoral artery catheter connected to a pressure transducer &#40;TruWave<span class="elsevierStyleSup">&#174;</span>&#44; Edwards Lifesciences LLC&#44; Irvine&#44; CA&#44; USA&#41;&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0125">Experimental protocol</span><p id="par0040" class="elsevierStylePara elsevierViewall">Immediately after the baseline measurement of hemodynamic and lung mechanics&#44; the animals were randomly assigned to the EPLS group &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>8&#41; or the EPHS group &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>8&#41;&#44; and the lung injury was induced by continuous intravenous infusion of OA &#40;0&#46;133<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> for 2<span class="elsevierStyleHsp" style=""></span>h&#41; via the central venous catheter&#46;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">11</span></a> During this period&#44; the EPLS group received 15<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> of Ringer Lactate&#44; and the EPHS group received 30<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#46; Once 2<span class="elsevierStyleHsp" style=""></span>h elapsed&#44; all of the rabbits were killed by an injection of a lethal dose of chloride potassium&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">At the end of the experiment&#44; the thorax was opened&#44; and the lungs were removed en bloc&#46; The right lung was weighed and then dried in a microwave oven at a power of 150<span class="elsevierStyleHsp" style=""></span>W for 60<span class="elsevierStyleHsp" style=""></span>min&#46;<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">20</span></a> The ratio of wet weight to dry weight &#40;WW&#47;DW&#41; of the right lung was calculated to assess tissue edema&#46; The left lung was excised and immersed in 10&#37; formaldehyde for at least 72<span class="elsevierStyleHsp" style=""></span>h&#46; Tissue samples were dehydrated with graded alcohol&#44; embedded in paraffin&#44; and cut in a series of 4<span class="elsevierStyleHsp" style=""></span>&#956;m-thick slices that were stained with hematoxylin and eosin&#46; A pathologist &#40;JRC&#41; then evaluated these tissue sections in a blinded fashion using the following scoring system to grade the degree of lung injury&#58; 0 &#40;no damage&#41; to 3 &#40;maximal damage&#41;&#46; These score were according to the combined assessments of alveolar congestion&#44; alveolar hemorrhage and edema&#44; infiltration&#47;aggregation of the neutrophils in the airspace or vessel wall&#44; the thickness of the alveolar wall&#44; bronchiole epithelial desquamation&#44; and hyaline membrane formation</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0130">Statistical analysis</span><p id="par0050" class="elsevierStylePara elsevierViewall">Unless otherwise indicated&#44; the results are presented as mean<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>SD&#46; Data were tested for normal distribution with the Agostino-Pearson test&#46; We used a two-way analysis of variance for repeated measures to determine the statistical significance of group differences in the respiratory parameters and the Doppler transesophageal measurements at different time points&#46; When statistical significance was indicated&#44; it was further examined by a post hoc analysis &#40;Student&#8211;Newman&#8211;Keuls test&#41;&#46; A Student&#39;s unpaired <span class="elsevierStyleItalic">t</span>-test was used for single-time point observation&#46; Results from the histological studies are expressed as median and range&#44; and the statistical analysis was performed using the Mann Whitney <span class="elsevierStyleItalic">U</span>-test&#46; Data were analyzed by using MedCalc Statistical Software &#40;version 9&#46;5&#46;2&#46;0&#59; MedCalc Software bvba&#44; Ostend&#44; Belgium&#41;&#46; Statistical significance was assumed at a probability &#60;0&#46;05&#46;</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0135">Results</span><p id="par0055" class="elsevierStylePara elsevierViewall">In 16 rabbits randomly allotted to each of the two groups &#40;EPLS and EPHS&#41;&#44; we found that at the beginning of the experiment&#44; each group had similar baseline characteristics for any of the hemodynamic and respiratory variables measured &#40;<a class="elsevierStyleCrossRefs" href="#tbl0005">Tables 1 and 2</a>&#41;&#46; The total fluid intake &#40;i&#46;e&#46;&#44; sedation&#44; oleic preparation&#44; and fluid therapy&#41; was 19&#46;8<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> in the EPLS group and 36&#46;2<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> in the EPHS group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;001&#41;&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0140">Hemodynamic changes</span><p id="par0060" class="elsevierStylePara elsevierViewall">As shown in <a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#44; both strategies shown different hemodynamic effects&#46; Compared with the baseline&#44; there was a decrease in the CI that reached statistical significance in the animals in the EPLS group&#59; however in the animals in the EPHS group&#44; the CI remained unchanged throughout the experiment&#46; Heart rate decreased significantly in the animals in the EPHS group&#44; and by the end of the experiment&#44; the cFT was significantly higher in the EPHS group &#40;<a class="elsevierStyleCrossRef" href="#fig0005">Fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0145">Respiratory changes</span><p id="par0065" class="elsevierStylePara elsevierViewall">As shown in <a class="elsevierStyleCrossRef" href="#fig0010">Fig&#46; 2</a>&#44; the two strategies had different effects on respiratory mechanics&#46; Compared to the baseline&#44; at 1 and 2<span class="elsevierStyleHsp" style=""></span>h &#40;end of experiment&#41;&#44; the <span class="elsevierStyleItalic">C</span><span class="elsevierStyleInf">dyn</span> had decreased significantly only in animals in the EPHS group&#46; Other measurements of respiratory mechanics&#44; <span class="elsevierStyleItalic">R</span><span class="elsevierStyleInf">awi</span>&#44; <span class="elsevierStyleItalic">R</span><span class="elsevierStyleInf">awe</span> and WOB&#44; increased more in the EPHS group&#44; although without statistical significance&#46; No animals in either group showed auto-PEEP&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0150">Lung edema and descriptive histology</span><p id="par0070" class="elsevierStylePara elsevierViewall">Pulmonary edema estimation by calculating the WW&#47;DW ratio was increased in the two groups&#44; but it was higher in the EPHS group than in the EPLS group &#40;6&#46;8<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>0&#46;8<span class="elsevierStyleHsp" style=""></span>g in the EPHS group and 5&#46;8<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>0&#46;8<span class="elsevierStyleHsp" style=""></span>g in the EPLS&#44; <span class="elsevierStyleItalic">p</span>&#58; 0&#46;02&#59; normal value in our laboratory &#8764;5<span class="elsevierStyleHsp" style=""></span>g&#41;&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">In all of the animals&#44; the lungs exhibited gross damage&#44; including edema with petechial hemorrhages on the surface&#59; however&#44; the lungs of the animals in the EPHS group exhibited more intense damage&#44; especially hemorrhages &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#46; The histological findings&#44; including alveolar congestion&#44; interstitial and alveolar infiltration&#47;aggregation of neutrophils&#44; alveolar membrane focal thickening&#44; alveolar edema or hemorrhage&#44; bronchiole epithelial desquamation&#44; and hyaline membranes were present in similar degrees in both groups &#40;lung injury score 8&#46;5<a class="elsevierStyleCrossRefs" href="#bib0235"><span class="elsevierStyleSup">7&#8211;11</span></a> in the EPHS group and 8&#46;5<a class="elsevierStyleCrossRefs" href="#bib0230"><span class="elsevierStyleSup">6&#8211;9</span></a> in the EPLS group&#59; <span class="elsevierStyleItalic">p</span>&#58; 0&#46;4&#41;&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia></span></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0155">Discussion</span><p id="par0080" class="elsevierStylePara elsevierViewall">The main finding of this experimental study is that a preemptive hemodynamic intervention by restricting the administration of fluids significantly slowed the progression of pulmonary edema and the decreased pulmonary compliance in OA-induced acute lung injury&#46; When fluids were administered more liberally to focus on ensuring the hemodynamic stability&#44; pulmonary edema progression was higher and <span class="elsevierStyleItalic">C</span><span class="elsevierStyleInf">dyn</span> decreased more than when fluids were infused in smaller quantities that were insufficient to prevent hemodynamic deterioration&#46; Therefore&#44; the EPHS proved useful to maintain hemodynamic stability&#44; but it was detrimental to the progression of pulmonary edema&#59; conversely&#44; the EPLS was successful in reducing the progression of pulmonary edema&#44; but it was not effective in preventing hemodynamic deterioration&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">ARDS is a catastrophic form of lung injury characterized in more than half of patients by diffuse alveolar damage with severe inflammation and high permeability protein-rich edema in the lungs&#46;<a class="elsevierStyleCrossRef" href="#bib0240"><span class="elsevierStyleSup">8</span></a> This syndrome produces results that are notoriously difficult to treat once the diagnosis is made and has an associated mortality approaching 40&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">21</span></a> Recent studies suggest that the development of lung damage represents a progression of pathology in the lung between the time of insult and the time at which ARDS criteria are met&#46;<a class="elsevierStyleCrossRefs" href="#bib0310"><span class="elsevierStyleSup">22&#44;23</span></a> During this period of time&#44; referred to by some as the silent phase&#44;<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">24</span></a> further attacks or impacts &#40;i&#46;e&#46;&#44; second hits&#41; frequently occur&#46; These attacks contribute to the gradual progression from initial mild-moderate lung injury to clinical ARDS&#46;<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">4&#8211;7</span></a> Most of the time&#44; the second hits are iatrogenic insults&#44; including transfusions&#44; mechanical ventilations with high tidal volumes&#44; delayed treatments of shock and infection&#44; and the inappropriate administration of fluids&#46; Because of the second hits favoring the progression from mild to severe lung injury fulfilling the criteria for ARDS with devastating respiratory failure&#44; there are reasons to believe that the prevention of these hits should result in a decrease in the incidence and severity of ARDS&#46;<a class="elsevierStyleCrossRef" href="#bib0225"><span class="elsevierStyleSup">5</span></a> In this regard&#44; we think that our results suggest that fluid administration&#44; even cautiously adjusted to maintain cardiac output&#44; might behave as a second hit influencing the progression of pulmonary edema and favoring the development of ARDS&#46;</p><p id="par0090" class="elsevierStylePara elsevierViewall">The relationship between the administration of fluids and the development of ARDS was already stated over 40 years ago during periods of war&#46; During these times&#44; it was observed that many patients who had suffered severe trauma were strongly raised with crystalloid solutions and were stabilized in the battle field&#46; Later in the hospital&#44; these patients developed a very severe hypoxemic respiratory failure due to pulmonary edema&#44; which often led to death&#46; This entity&#44; called &#8220;wet lung&#8221;&#44;<a class="elsevierStyleCrossRefs" href="#bib0325"><span class="elsevierStyleSup">25&#44;26</span></a> at autopsy was characterized by histopathological changes similar to those described later in ARDS&#46;<a class="elsevierStyleCrossRefs" href="#bib0335"><span class="elsevierStyleSup">27&#44;28</span></a> In the civil stage&#44; several studies have reported a relationship between a positive fluid balance and the development of ARDS<a class="elsevierStyleCrossRefs" href="#bib0345"><span class="elsevierStyleSup">29&#8211;33</span></a>&#59; however&#44; to date&#44; there is a widespread opinion that it is difficult to establish whether or not this relationship represents a simple association or a cause-and-effect relationship&#46;<a class="elsevierStyleCrossRef" href="#bib0370"><span class="elsevierStyleSup">34</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">During the onset of lung injury and the development of diffuse alveolar damage&#44; high permeability pulmonary edema has a central role&#44; acting as a driving force that reduces the airspace available for normal gas exchange and contributes to the disruption of surfactant&#44; which leads to alveolar instability and collapse&#46; Pulmonary edema is determined by the Starling relationship&#44; which predicts the net flow of liquid across a membrane&#46; In acute lung injury&#44; the most common mechanism for a rise in the transcapillary filtration of fluids is an increase in capillary permeability&#46;<a class="elsevierStyleCrossRef" href="#bib0375"><span class="elsevierStyleSup">35</span></a> However&#44; experimental studies demonstrated that&#44; at a given increase in capillarity permeability&#44; a modest change in pulmonary vascular pressure greatly modifies the quantity of pulmonary edema&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">9</span></a> That is probably why a strategy of restricting the administration of fluids has demonstrated to be useful in acute lung injury for decreasing pulmonary edema and improving lung function&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">10</span></a> The novelty of our study is that&#44; when this strategy of restricting the administration of fluids was used at the very inception of the injury and pulmonary inflammation&#44; there was less pulmonary edema and less affectation of the respiratory mechanics&#46;</p><p id="par0100" class="elsevierStylePara elsevierViewall">On the other hand&#44; the strategy based on restricting the fluid administration&#44; inadequately maintained cardiac output&#46; The main hemodynamic consequences of OA infusion are a sharp increase in pulmonary vascular resistance with the elevation of pulmonary artery pressure and a significant decline in cardiac output and heart rate&#46;<a class="elsevierStyleCrossRef" href="#bib0380"><span class="elsevierStyleSup">36</span></a> Moreover&#44; depending of the doses and the velocity of OA administration&#44; systemic vascular collapse can develop&#46; To reverse the cardiac consequences of OA administration&#44; energetic fluid infusion and&#47;or inotropic drugs are frequently used&#46; For results in the benefits&#44; the fluid administration must increase the heart preload&#44; thereby increasing the systolic volume and the cardiac output&#46; In addition to the cardiac output&#44; transesophageal Doppler measurements include the cFT&#44; a parameter that&#44; although is influenced by the afterload&#44; has been proposed as a value of the preload&#46;<a class="elsevierStyleCrossRefs" href="#bib0290"><span class="elsevierStyleSup">18&#44;37</span></a> By the end of experiment&#44; the cFT was higher in the EPHS group&#44; and therefore&#44; we believe that the animals in the EPHS group maintained cardiac output&#44; at least during the second hour of the experiment&#44; mainly by increasing the cardiac preload&#46; However&#44; the importance of maintaining the cardiac output during ARDS development is not well known&#46; Although adequate cardiac output is necessary to ensure enough oxygen delivery&#44; high cardiac output can be detrimental for lung injury enhancing transcapillary filtration and pulmonary edema&#46;<a class="elsevierStyleCrossRef" href="#bib0390"><span class="elsevierStyleSup">38</span></a> Therefore&#44; it is possible that in our experiment&#44; a slight decrease in the cardiac output in the animals in the EPLS group was useful to protect the lungs&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">In addition to the experimental nature of this study&#44; there are some limitations to our study&#46; First&#44; the lung injury model we used&#46; Although OA administered to animals increases pulmonary vascular permeability and produces a condition that pathophysiologically resembles acute lung injury in humans&#44;<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">13</span></a> the severity or extensiveness of the injury depends on the doses and the direction of the OA administration&#58; a simple bolus&#44; repeated injections&#44; or a continuous infusion&#46; We chose a model by a slow and steady infusion of OA for 2<span class="elsevierStyleHsp" style=""></span>h<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">11</span></a> that provides a better hemodynamic tolerance and allows for the monitoring of hemodynamic and respiratory changes in detail&#46; However&#44; when the OA is administered in this way&#44; lung damage may progress for at least 6<span class="elsevierStyleHsp" style=""></span>h&#46;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">11</span></a> Therefore&#44; it is very likely that the short duration of our study prevented the full development of lung injury in both of the groups&#46; Another important aspect of the study is the way in which the fluids were administered&#46; For the EPHS group&#44; we selected a set amount of fluid to keep CI based on previous preliminary observations we made in our laboratory&#46; However&#44; it is possible that the animals in the EPHS group received an excessive and inadequate amount of fluids&#44; and a component of overhydration was present&#46; Obviously the inclusion of a sham group could have helped to clarify this issue&#46; With respect to the measurement of cardiac output by oesophageal Doppler there is little experience about precision in small animals&#44;<a class="elsevierStyleCrossRef" href="#bib0395"><span class="elsevierStyleSup">39</span></a> but we believe that a previous analysis published by our own group<a class="elsevierStyleCrossRef" href="#bib0400"><span class="elsevierStyleSup">40</span></a> strongly supports the accuracy of the reported differences in CI between the two groups&#46; Finally&#44; although we graded the histopathologic findings using a scoring system&#44; we did not perform an extensive study&#46; The fact that there was more macroscopic involvement in the lungs of the EPHS group &#40;<a class="elsevierStyleCrossRef" href="#fig0015">Fig&#46; 3</a>&#41;&#44; raises the question that the histological damage was also more extensive in this group&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">In conclusion&#44; the results of our study entrench a cause-and-effect relationship between fluids and the development of pulmonary edema at the beginning of acute lung injury with diffuse alveolar damage and demonstrate that&#44; at the very inception of the injury and the pulmonary inflammation&#44; an early strategy of restricting the infusion of fluids is associated with a reduction in the progression of pulmonary edema and the deterioration of lung mechanics&#46; Thus&#44; we believe that in a clinical setting with patients at risk of developing ARDS a strategy of restricting the administration of fluids should be investigated&#46;</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0160">Funding</span><p id="par0115" class="elsevierStylePara elsevierViewall">This study did not receive any funding after being rejected twice by the Ministry of Health of the Government of Andalusia in 2008 calls &#40;PI-0174&#41; and 2009 &#40;PI-0264&#41;&#46;</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0165">Conflict of interests</span><p id="par0120" class="elsevierStylePara elsevierViewall">Anselmo Gil Cano has received Honoraria from Edwards Lifesciences&#46; Manuel Ignacio Monge Garc&#237;a was consultant for Edwards Lifesciences and received travel expenses from Deltex&#46; Manuel Gracia Romero&#44; Pedro Guijo Gonz&#225;lez and Jos&#233; Ruiz Campos have no conflict of interest to declare&#46;</p></span></span>"
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              "titulo" => "Hemodynamic changes"
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              "titulo" => "Lung edema and descriptive histology"
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    "fechaRecibido" => "2016-05-25"
    "fechaAceptado" => "2016-08-03"
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            0 => "Acute lung injury"
            1 => "Oleic acid"
            2 => "Second hits"
            3 => "Early protective lung strategy"
            4 => "ARDS"
            5 => "Pulmonary edema"
            6 => "Respiratory mechanics"
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            0 => "Lesi&#243;n pulmonar aguda"
            1 => "&#193;cido oleico"
            2 => "Impactos secundarios"
            3 => "Estrategia precoz protectora pulmonar"
            4 => "SDRA"
            5 => "Edema pulmonar"
            6 => "Mec&#225;nica respiratoria"
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        "titulo" => "Abstract"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Objective</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">A study is made of the influence of preemptive hemodynamic intervention restricting fluid administration upon the development of oleic acid-induced lung injury&#46;</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Design</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">A randomized in vivo study in rabbits was carried out&#46;</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Setting</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">University research laboratory&#46;</p></span> <span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Subjects</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Sixteen anesthetized&#44; mechanically ventilated rabbits&#46;</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Variables</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Hemodynamic measurements obtained by transesophageal Doppler signal&#46; Respiratory mechanics computed by a least square fitting method&#46; Lung edema assessed by the ratio of wet weight to dry weight of the right lung&#46; Histological examination of the left lung&#46;</p></span> <span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Interventions</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Animals were randomly assigned to either the early protective lung strategy &#40;EPLS&#41; &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>8&#41; or the early protective hemodynamic strategy &#40;EPHS&#41; &#40;<span class="elsevierStyleItalic">n</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>8&#41;&#46; In both groups&#44; lung injury was induced by the intravenous infusion of oleic acid &#40;OA&#41; &#40;0&#46;133<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> for 2<span class="elsevierStyleHsp" style=""></span>h&#41;&#46; At the same time&#44; the EPLS group received 15<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span> of Ringer lactate solution&#44; while the EPHS group received 30<span class="elsevierStyleHsp" style=""></span>ml<span class="elsevierStyleHsp" style=""></span>kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#46; Measurements were obtained at baseline and 1 and 2<span class="elsevierStyleHsp" style=""></span>h after starting OA infusion&#46;</p></span> <span id="abst0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Results</span><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">After 2<span class="elsevierStyleHsp" style=""></span>h&#44; the cardiac index decreased in the EPLS group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#44; whereas in the EPHS group it remained unchanged&#46; Lung compliance decreased significantly only in the EPHS group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#46; Lung edema was greater in the EPHS group &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#46;05&#41;&#46; Histological damage proved similar in both groups &#40;<span class="elsevierStyleItalic">p</span><span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#46;4&#41;&#46;</p></span> <span id="abst0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Conclusions</span><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">In this experimental model of early lung injury&#44; lung edema progression was attenuated by preemptively restricting the administration of fluids&#46;</p></span>"
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        "resumen" => "<span id="abst0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Objetivo</span><p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Conocer c&#243;mo influye una intervenci&#243;n hemodin&#225;mica preventiva basada en la restricci&#243;n de fluidos sobre el desarrollo de la lesi&#243;n pulmonar inducida por la administraci&#243;n de &#225;cido oleico&#46;</p></span> <span id="abst0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Dise&#241;o</span><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">Estudio aleatorizado en animales vivos&#46;</p></span> <span id="abst0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">Lugar</span><p id="spar0055" class="elsevierStyleSimplePara elsevierViewall">Laboratorio universitario de investigaci&#243;n experimental&#46;</p></span> <span id="abst0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Variables</span><p id="spar0060" class="elsevierStyleSimplePara elsevierViewall">Mec&#225;nica respiratoria &#40;m&#233;todo de los m&#237;nimos cuadrados&#41;&#44; medidas hemodin&#225;micas &#40;doppler esof&#225;gico&#41;&#44; estimaci&#243;n del edema pulmonar &#40;relaci&#243;n peso h&#250;medo&#47;seco del pulm&#243;n derecho&#41; y da&#241;o histol&#243;gico del pulm&#243;n izquierdo&#46;</p></span> <span id="abst0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Intervenciones</span><p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Ocho animales fueron asignados a un grupo con una estrategia protectora pulmonar &#40;EPP&#41;&#44; y otros 8 a otro grupo con una estrategia protectora hemodin&#225;mica &#40;EPH&#41;&#46; En ambos grupos la lesi&#243;n pulmonar se desencaden&#243; mediante la administraci&#243;n intravenosa de &#225;cido oleico &#40;0&#44;133<span class="elsevierStyleHsp" style=""></span>mL&#47;kg<span class="elsevierStyleSup">&#8722;1</span>&#47;h<span class="elsevierStyleSup">&#8722;1</span> durante 2<span class="elsevierStyleHsp" style=""></span>h&#41;&#44; recibiendo simult&#225;neamente los animales del grupo EPP 15<span class="elsevierStyleHsp" style=""></span>mL&#47;kg<span class="elsevierStyleSup">&#8722;1</span>&#47;h<span class="elsevierStyleSup">&#8722;1</span> de Ringer Lactato y los del grupo EPH 30<span class="elsevierStyleHsp" style=""></span>mL<span class="elsevierStyleHsp" style=""></span>Kg<span class="elsevierStyleSup">&#8722;1</span><span class="elsevierStyleHsp" style=""></span>h<span class="elsevierStyleSup">&#8722;1</span>&#46; Se obtuvieron medidas basales&#44; a la hora y a las 2<span class="elsevierStyleHsp" style=""></span>h&#46;</p></span> <span id="abst0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Resultados</span><p id="spar0070" class="elsevierStyleSimplePara elsevierViewall">Transcurridas las 2<span class="elsevierStyleHsp" style=""></span>h de experimento el &#237;ndice cardiaco permaneci&#243; estable en el grupo EPH&#44; pero disminuy&#243; en el grupo EPP &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#46; Por el contrario&#44; la distensibilidad pulmonar disminuy&#243; significativamente solo en el grupo EPH &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#44; en el cual el edema pulmonar estimado mediante la relaci&#243;n peso h&#250;medo&#47;seco del pulm&#243;n derecho fue mayor &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#46; El da&#241;o histol&#243;gico fue similar en ambos grupos &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;4&#41;&#46;</p></span> <span id="abst0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Conclusiones</span><p id="spar0075" class="elsevierStyleSimplePara elsevierViewall">En este modelo experimental de lesi&#243;n pulmonar aguda en fase inicial&#44; la formaci&#243;n del edema pulmonar fue atenuada por la restricci&#243;n preventiva en la administraci&#243;n de fluidos&#46;</p></span>"
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Idiomas
Medicina Intensiva (English Edition)
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¿Es usted profesional sanitario apto para prescribir o dispensar medicamentos?

Are you a health professional able to prescribe or dispense drugs?