Role of l-arginine in preventing myocardial and endothelial injury following ischaemia/reperfusion in the rat isolated heart

The protective effect of l -arginine on ischaemia/reperfusion-induced myocardial injury was investigated in the rat isolated Langendorff perfused heart. Six groups of hearts subjected to 30 min global ischaemia and 30 min reperfusion received either vehicle, d -arginine, l -arginine, the nitric oxide (NO)-donor S-Nitroso-N-Acetyl-d, l -Penicillamine (SNAP), the inhibitor of NO formation N^G-nitro-l -arginine (l -NNA), or l -arginine plus l -NNA. The recoveries of left ventricular double product and coronary flow at the end of reperfusion were significantly higher in the l -arginine group (85±5 and 75±6%, respectively) than in the vehicle group (37±6 and 34±5%, respectively, P<0.05). During both the ischaemic and reperfusion periods, left ventricular end diastolic pressure was lower in the l -arginine group than in the vehicle group. Creatine kinase outflow and the area of no-reflow were smaller in the l -arginine treated hearts (P<0.01). There were no differences between vehicle and d -arginine treated groups. l -NNA did not affect recovery per se but abolished the protective actions of l -arginine. SNAP produced the same protective effects as l -arginine. Acetylcholine-induced endothelium-dependent vasodilation was reduced after ischaemia and reperfusion in the vehicle group but not in the l -arginine group. It is concluded that l -arginine reduces ischaemia/reperfusion-induced myocardial and endothelial injury. The results suggest that the beneficial effects of l -arginine are related to preserved synthesis and release of NO.