ABSTRACT
Reperfusion of ischemic myocardium has been reported to cause rapid degeneration of endothelial function, characterized by a decreased release of NO in response to endothelium-dependent vasodilators. A previous study showed that NO donors given during reperfusion preserve coronary artery ring vasorelaxation and reduce myocardial injury associated with ischemia and reperfusion. A study by Engelman et al. (1995) evaluated whether the NO precursor, L-Arg, could reduce ischemia/ reperfusion injury by preventing leukocyte-endothelial interactions. Th ey induced regional ischemia in an open-chest pig heart for 30 min followed by 90 min of reperfusion. A preischemic 10-min intravenous infusion of 4 mg/kg/min of Arg was compared to control pigs. Th e results showed that L-Arg administration reduced plasma levels of ICAM-1, E-selectin, and VCAM-1. Myocardial stunning and arrhythmias were also reduced. A study by Hayashida et al. (2000) investigated the eff ect of Arg on myocardial reperfusion injury. Isolated hearts were perfused with blood at 37°C from a support rat. Aft er 20 min of aerobic perfusion, the hearts were arrested for 60 min with warm blood cardioplegia given at 20 min intervals. Th is was followed by 60 min of reperfusion. Th e hearts were divided into three groups according to the supplemental drugs added to the cardioplegic solution. Th e control group received warm-blood cardioplegia. Th e Arg group received warm blood supplemented with Arg, and the third group received warm blood supplemented with Arg and NG-nitro-L-arginine methyl ester (L-NAME, an iNOS inhibitor). Th e results showed that compared to the other two groups, the Arg group showed early recovery of lactate metabolism and greater coronary blood fl ow during reperfusion. Levels of myocardial release of circulating ICAM-1 and E-selectin were lower in the Arg group.
