Abstract
The coronary artery disease is a leading cause of death and morbidity worldwide. This disease has a complex pathophysiology that includes multiple mechanisms. Among these is the oxidative/nitrosative stress. Paradoxically, oxidative/nitrosative signaling plays a major role in cardioprotection against ischemia/reperfusion injury. In this context, the gas transmitter nitric oxide may act through several mechanisms, such as guanylyl cyclase activation and
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