Intestinal Preconditioning Ameliorates Ischemia-Reperfusion Induced Acute Lung Injury in Rats: An Experimental Study

BackgroundPhospholipases A2 (PLA2) have been implicated in the pathogenesis of acute respiratory distress syndrome (ARDS) induced by intestinal ischemia-reperfusion (IIR). Intestinal ischemic preconditioning (IIP) has been shown to improve intestinal tolerance to subsequent sustained ischemia and limit the systemic inflammatory response. We tested the effect of IIP on the intestinal ischemia-reperfusion-induced ARDS, with particular focus on PLA2.MethodsRats were randomized into three groups: (1) sham surgery group (sGroup), 45 min sham intestinal ischemia–4 h reperfusion, (2) IIR group (IIRGroup), 45 min intestinal ischemia–4 h reperfusion, (3) IIP group (ipGroup), three cycles of intestinal ischemia for 4 min and reperfusion for 10 min followed by 45 min intestinal ischemia–4 h reperfusion. At the end of each experiment, blood gases were obtained and bronchoalveolar lavage (BAL) followed. Biochemical (total protein, PLA2, PAF-AcH) and cytological parameters of the BAL fluid were quantified. Plasma MDA was measured as an indicator of systemic oxidative stress. Comparisons between groups were made using one-way ANOVA followed by post hoc comparison with a Tukey test or Mann-Whitney test when appropriate. Differences were considered significant if P < 0.05.ResultsAlveolar-arterial O2 gradient values and wet to dry lung ratio were significantly (P < 0.05) increased in the IIRGroup and this increase was prevented in the ipGroup. Following the same pattern, BAL total protein, PLA2, and PAF-AcH were significantly lower in the ipGroup. Ischemic preconditioning significantly abolished neutrophil count in BAL fluid. Plasma MDA was significantly lower in the ipGroup. Despite a significant tissue polymorphonuclear reduction, no significant lung or intestinal histologic damage score changes were revealed.ConclusionsIntestinal preconditioning protects IIR-induced lung injury, partly by modulating the arachidonic acid cascade.