The role of nitric oxide in cardiac surgery.
The release of nitric oxide (NO) from coronary endothelial cells is impaired following reperfusion; however, several experimental studies have found that it exerts a cardioprotective effect during myocardial ischemia-reperfusion. Thus, attempts have been made to supplement NO production exogenously during reperfusion when endogenous NO release may be diminished. Conversely, other studies suggest that NO exacerbates reperfusion injury by inducing the production of peroxynitrite. NO has also been reported to provide beneficial effects as a selective pulmonary vasodilator to relieve pulmonary hypertension. A loss of NO-mediated relaxation caused by the dysfunction of endothelial cells is characteristic of intimal hyperplasia, and nitrosovasodilators have proven efficient against atherosclerotic coronary heart disease, which may be attributable to their antiplatelet effects as well as to vasodilation. Furthermore, protamine sulfate, which is rich in L-arginine, is thought to augment NO production by supplying exogenous L-arginine, or to act on endothelial cell receptors to stimulate the production of NO. This review summarizes the current role of NO in cardiac surgery.
Nonami
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Department of Surgery II, Kochi Medical School, Japan.
D000818:Animals; D001120:Arginine / Q000502:physiology; D006348:Cardiac Surgical Procedures; D004195:Disease Models, Animal; D006331:Heart Diseases / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D006976:Hypertension, Pulmonary / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D017202:Myocardial Ischemia / Q000503:physiopathology; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D018375:Neutrophil Activation; D009569:Nitric Oxide / Q000502:physiology* / Q000627:therapeutic use; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D014664:Vasodilation / Q000502:physiology
D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase