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Increased levels of reactive oxygen species, alterations in nitric oxide synthesis, and increased migration of neutrophils to the ischemic tissue play an important role in the pathophysiology of myocardial ischemia-reperfusion (IR) injury. In this study, we have evaluated the effects of melatonin on myeloperoxidase (MPO) activity, tissue glutathione (GSH), lipid peroxidation levels, and blood pressure in L-NAME-induced hypertensive rats with or without IR. NOS inhibitor L-NAME was administrated before inducing cardiac ischemia for 15 days intraperitoneally. For the cardiac ischemia, the left coronary artery was ligated for 30 min, and reperfusion was performed for 120 min after the ischemia. L-NAME treatment in non-ischemic animals increased blood pressure and lipid peroxidation, and decreased glutathione level in myocardial tissue significantly as compared with non-L-NAME-treated animals. Melatonin reversed L-NAME-induced blood pressure elevation and oxidative changes. Cardiac IR increased MDA levels and MPO activity and decreased GSH levels as compared with non-ischemic animals. L-NAME treatment did not change in IR-induced MDA and GSH levels as compared with ischemic control animals. However, MPO activity was significantly higher than control ischemic animals. MDA levels and MPO activity resulting from ischemic injury in melatonin-treated animals were significantly less than L-NAME-treated animals. Taken together-the ischemic and non-ischemic control and melatonin-treated animals-this study shows that neutrophil migration plays an important role on the development of ischemic injury in hypertensive rats.

Reduction in the synthesis or bioavailability of nitric oxide plays a significant role in the development of myocardial infarction and hypertension. Numerous studies suggest that melatonin reduces blood pressure (BP) and ischemia/reperfusion (I/R) injury in rats. The effects of melatonin on the BP and I/R-induced cardiac infarct size in L-NAME-induced hypertensive rats remains unknown. This study was designed to investigate the effects of melatonin on BP and the I/R-induced infarct size in chronic nitric oxide synthase inhibited rats by L-NAME. Rats received L-NAME for 15 days to produce hypertension and melatonin the last 5 days before I/R studies. To produce cardiac damage, the left coronary artery was occluded for 30 min, followed by 120 min reperfusion. L-NAME led to a significant increase in BP. Melatonin administration (10 mg/kg) to L-NAME treated rats significantly reduced BP and infarct size. Also, melatonin attenuated the mortality resulting from I/R, but this was not statistically significant. Melatonin administration would seem important to reduce BP and infarct size resulting from I/R in L-NAME-induced hypertensive rats.

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