The Role of Nitric Oxide in Cardiac Ischemia-Reperfusion Injury

Abstract

During cardiac surgery, ischemia-reperfusion injury (IRI) is thought to be a major factor in intraoperative myocardial damage. Coronary endothelial cells have been thought to play an important role in the pathogenesis of cardiac IRI. Release of nitric oxide (NO) from coronary endothelial cells is impaired following myocardial ischemia, and this may contribute to the vulnerability of the coronary circulation to thrombus-formation and vasospasm. Several experimental studies have found that NO has a cardioprotective effect in myocardial IRI. In this regard, attempts have been made to supplement NO production exogenously during reperfusion, when endogenous NO release from endothelial cells may be diminished. In a blood-reperfused heart model, L-arginine acts cardioprotectively via 2 primary possible mechanisms: (1) by blocking both neutrophil aggregation and neutrophil adherence, and (2) by scavenging oxygen-derived free-radicals. On the other hand, in a non-blood reperfused heart model, the optimal concentration of L-arginine may be low and protection may be due to 2 additional mechanisms: (3) direct coronary vasodilatation and (4) reduced oxygen demand due to vasodilatation-induced hypotension. Other studies have suggested that NO exacerbates IRI and that NO synthase (NOS) inhibitors act cardioprotectively. It has also been suggested that the pharmacological effectiveness of inhibiting NO production may be due to the prevention of peroxinitrite formation from NO and superoxide during reperfusion. This review summarizes the current understanding of the role of NO in IRI.

Antiarrhythmic effect of heat adaptation in ischemic and reperfusion injury to the heart

“…These specific features were probably related to high activity of antioxidant systems in the organism that play a role in myocardial protection from reperfusion injury. Our hypothesis is confirmed by published data that NO activates expression of genes for antioxidant enzymes [11]. It cannot be excluded that the development of late reperfusion arrhythmias is associated with apoptosis in myocardial cells, which results from free radical generation under conditions of oxygen supply to damaged heart tissue [10,12].…”

Antioxidant screening of medicinal herbal teas

“…Finally, our interest in assessing the peroxynitritequenching activity of herbal teas stems from the apparent involvement of peroxynitrite anions in the ethiogenesis of pathologies associated with ischemiareperfusion injury (Nonami, 1997), and in the oxidation of LDL (Carr et al, 2000), a key atherogenic event.…”

Protective effects of L-arginine on pulmonary oxidative stress and anti-oxidant defenses during exhaustive exercise in rats1

“…Numerous studies have shown that L-Arg is a precursor of NO, which can increase coronary vasodilation, scavenge various free radicals, inactivate Fe-S centers of XO and suppress XO activity as well as inhibit platelet and neutrophil adhesion to the endothelium [33,34] . Hence, the protective role of NO is probably a result of its ability to scavenge free radicals, reduce lipid peroxidation, and inhibit XO, which are in accordance with our results for the E+Arg group.…”