DIFFERENTIAL-EFFECTS OF N-ACETYLCYSTEINE ON NITROGLYCERIN-INDUCED ANDNICORANDIL-INDUCED VASODILATION IN HUMAN CORONARY CIRCULATION

We investigated the role of the availability of sulfhydryl groups duri ng vasodilation of the human coronary circulation induced by nitroglyc erin and nicorandil. In patients with normal coronary arteries (n = 29 ) or with coronary artery disease (CAD; n = 26), coronary blood flow ( CBF) and epicardial coronary artery diameter after intracoronary admin istration of 50 mu g nitroglycerin or 0.5 mg nicorandil were measured, before and after the intravenous infusion of saline or 100 mg/kg of N -acetylcysteine (NAC). In normal subjects, saline infusion did not alt er the nitroglycerin-and nicorandil-induced vasodilation in large epic ardial coronary artery. In contrast, NAC potentiated both nitroglyceri n-and nicorandil-induced vasodilation. In patients with CAD, nitroglyc erin and nicorandil induced less dilation than in normal subjects. NAC augmented the nitroglycerin- and nicorandil-induced vasodilation in t he small epicardial coronary artery, but not in the large epicardial s egments. In both groups, NAC potentiated the increase in CBF in respon se to nitroglycerin. However, NAC had no effects on the CBF response t o nicorandil. Sulfhydryl availability is at least one determinant of t he in vivo responsiveness to nitroglycerin of conductance and resistan ce vessels in normal human coronary circulation. In patients with CAD, external augmentation of sulfhydryl availability did not affect the d epressed response to nitroglycerin in the large epicardial coronary ar tery. Although nicorandil acts as an NO donor, similar to nitroglyceri n, in dilating the epicardial coronary artery, other effects, such as the opening of K-ATP channel, play a more important role in the nicora ndil-induced vasodilation of resistance vessels.