Ischemia postconditioning preventing lung ischemia-reperfusion injury

Objective: This study evaluates the inhibitory effect of IPO against ischemia reperfusion (I/R) induced lung injury in rats. Methods: Anesthetized and mechanically ventilated adult Sprague Dawley rats were randomly assigned to one of the following groups (n = 12 each): the sham operated control group, the ischemia reperfusion (IR) group (30 min of left-lung ischemia and 24 h of reperfusion), the IPO group (three successive cycles of 30-s reperfusion per 30-s occlusion before restoring full perfusion), and the dexamethasone plus IPO group (rats were injected with dexamethasone (3 mg/kg.day(-1)) 10 min prior to the experiment and the rest of the procedures were the same as the IPO group). Lung injury was assessed by wet-to-dry lung weight ratio and tissue apoptosis and biochemical changes. Results: Lung ischemia reperfusion increased lung MDA production, serum proinflammatory cytokine count, and MPO activity and reduced antioxidant enzyme activities (all p < 0.05 I/R versus sham), accompanied with a compensatory increase in caspase-3, bax,Fas, FasL proteins and a decrease in Bcl-2 protein. Plasma levels of TNF-alpha, IL-6, and IL-1 beta were increased in the I/R group (all p < 0.05 versus sham). IPO attenuated or prevented all the above changes. Treatment with dexamethasone enhanced all the protective effects of postconditioning. Conclusion: Postconditioning obviously inhibits I/R induced lung injury by its antioxidant anti-inflammatory and anti-apoptosis activities. (C) 2014 Elsevier B.V. All rights reserved.