Study of the Role of Nitric Oxide in Cardiac Performance during Experimental Ischemic Cardiac Arrest and Reperfusion

Abstract

The generation of up to ≈70% of systemic nitric oxide (NO) is accomplished by endothelial nitric oxide synthase (eNOS), one of 3 members of the NOS family of enzymes (other enzymes: neuronal nitric oxide synthase nNOS and inducible nitric oxide synthase iNOS) (Xia et al., 1996). The function of synthesized endothelial NO is to accomplish vasodilation, blood pressure regulation, inhibition of platelet aggregation and inhibition of endothelial inflammatory cell recruitment (Lundberg et al., 2008). Normal production of NO may prevent various types of cardiovascular disease, including, atherosclerosis, stroke, and hypertension (Bryan N. 2006). In this respect Rajwa Taher (2007) developed an experimental model of hypertension by administration of L-NAME, an inhibitor of NO synthase. Combined administration of L-arginine with L-NAME could prevent the induction of L-NAME hypertension (Taher et al., 2007). Coronary heart disease is a growing problem in most of the developing regions of the world and the most common mode of cardiovascular deaths is ischemic heart disease and stroke (Gersh et al., 2010). Acute myocardial infarction can be considered a leading cause of morbidity and mortality in the world (Mozaffarian et al., 2016).