s-nitro-n-acetylpenicillamine and Coronary-Artery-Disease

We examined the role of nitric oxide (NO) in ischemia-reperfused hearts. In an occlusion-reperfusion model of hypercholesterolemic rabbits, the extent of myocardial infarction was increased because of the activation of neutrophils, possibly due to the impaired production of NO in atherosclerotic coronary circulation. It was reversed by the addition of exogenous NO releaser, SNAP. In a hypoxia-reoxygenation model of cultured cardiac myocytes, NO produced by endogenous cardiac iNOS augmented myocyte injury after exposure to hypoxia-reoxygenation. Inhibition of glutathione peroxidase activity was suggested to be the mechanism of sensitization to oxidative stress after exposure to NO. Therefore, NO is supposed to play two roles in ischemia-reperfused hearts, i.e., cardioprotective effect through coronary circulation and cardiotoxic effect through direct action on cardiac myocytes.

Topics: Animals; Cells, Cultured; Coronary Artery Disease; Depression, Chemical; Glutathione Peroxidase; Myocardial Infarction; Myocardial Reperfusion Injury; Myocardium; Nitric Oxide; Oxidative Stress; Penicillamine; Rabbits