Inhibition of nitric oxide does not affect reperfusion-induced myocardial injury, but it prevents lipid peroxidation in the isolated rat heart.

To examine if inhibition of nitric oxide (NO) synthesis influences myocardial ischemia-reperfusion injury, male Sprague Dawley rats were administered the NO synthesis inhibitor N -nitro-L-arginine methyl ester (L-NAME, 10 mg/kg, i.p.) or saline 6 hours prior to excising the heart and aorta. Aortic ring contractile response to norepinephrine (NE) was more pronounced and relaxation in response to acetylcholine was abolished in L-NAME-treated group (P<0.05 vs. saline-treated group), indicating inhibition of NO synthesis in the vascular tissues. In the isolated perfused Langendorff hearts, force of cardiac contraction (FCC) and coronary perfusion pressure (CPP) were higher and coronary flow was lower in the L-NAME-treated group, again suggesting inhibition of NO synthesis. Global ischemia (40 min) followed by reperfusion (30 min) resulted in a decrease in FCC and coronary flow and an increase in CPP in all hearts. Myocardial CK also decreased similarly in all hearts. However, ischemia-reperfusion-induced decline in myocardial superoxide dismutase (SOD) activity and increase in malondialdehyde were prevented in the L-NAME-treated group (P<0.01 vs. saline-treated hearts). Thus treatment with L-NAME with resultant inhibition of NO synthesis does not affect ischemia-reperfusion-induced cardiac dysfunction and injury in the isolated rat hearts, although the reduction in SOD activity and the rise in lipid peroxidation following reperfusion are attenuated.