Remote postconditioning induced by brief pulmonary ischemia and reperfusion attenuates myocardial reperfusion injury in rabbits.

Background: The lung is one of the most important organs that are sensitive to ischemia. We hypothesized that remote postconditioning (RPostC) induced by brief occlusion and reperfusion of the pulmonary artery could attenuate myocardial reperfusion injury.

Methods: Thirty rabbits were randomized into three groups. Group ischemia-reperfusion (IR) (n = 10) were anesthetized rabbits subjected to 30-minute occlusion of the left anterior descending coronary artery followed by 180-minute reperfusion. Group RPostC (n = 10) had the left pulmonary artery blocked for five minutes followed by a 5-minute reperfusion, and the left anterior descending coronary artery (LAD) occluded for 30 minutes with a 180-minute reperfusion. Group L-N(w)-nitro-L-arginine methylester (L-NAME) + RPostC (n = 10) had the left pulmonary artery blocked for five minutes followed by a 5-minute reperfusion and intravenous infusion of L-NAME (10 mg/kg), and the LAD occluded for 30 minutes with a 180-minute reperfusion. Blood samples were taken for levels of creatine kinase (CK), superoxide dismutase (SOD) and malondialdehyde (MDA) at three different time points. At the end of the experiment, tissue samples of the infarcted region were harvested to calculate the cardiomyocyte apoptosis index (AI) by TUNEL. A piece of left and right lung tissue was harvested to evaluate the damage to the lung.

Results: After reperfusion for 180 minutes, the concentration of CK was lower in group RPostC, (4.79 ± 0.27) U/ml, than that in group IR, (6.23 ± 0.55) U/ml (P < 0.01), and group L-NAME + RPsotC, (5.86 ± 0.42) U/ml (P < 0.01). The concentration of MDA was lower in group RPostC, (6.06 ± 0.36) nmol/ml, than that in group IR, (11.41 ± 0.91) nmol/ml (P < 0.01), and group L-NAME + RPostC, (11.06 ± 0.62) nmol/ml (P < 0.01). The activity of SOD was higher in group RPostC, (242.34 ± 25.02) U/ml, than that in group IR, (148.05 ± 18.24) U/ml (P < 0.01), and group L-NAME + RPostC, (160.66 ± 9.55) U/ml (P < 0.01). The apoptosis index was lower in group RPostC, (14.25 ± 5.20)%, than that in group IR, (35.77 ± 10.09)% (P < 0.01), and group L-NAME + RPostC, (30.37 ± 7.76)% (P < 0.01). No significant difference caused by pulmonary ischemia was found in the lung tissue among the three groups.

Conclusions: RPostC may attenuate myocardial ischemia-reperfusion injury connected to the activity of endothelial nitric oxide synthase. Brief pulmonary ischemia may not be harmful to lungs.