Ethanol causes epicardial coronary artery vasoconstriction in the intact dog

Ethanol produces in vitro vasoconstriction of coronary arteries and can precipitate angina in patients with coronary obstructive disease. To demonstrate the in vivo effect of ethanol on coronary dynamics, baseline measurements of left anterior descending (LAD) coronary artery dimension by quantitative angiography, hemodynamics, arterial and coronary sinus blood gases, and blood ethanol levels were obtained in 14 closed-chest mongrel dogs. Three ethanol levels were established by intravenous bolus followed by 1-hour maintenance infusions. All measurements made at baseline were recorded every 30 minutes. Phentolamine (5 mg i.v.) and nicardipine (0.15 mg/kg i.v.) were given to evaluate constrictor mechanisms. Blood ethanol levels achieved at 60, 120, and 180 minutes were 649 ± 48, 1,285 ± 81, and 2,546 ± 130 μg/ml, respectively. LAD cross-sectional area was reduced significantly from control at the end of each of the three dosing periods (-24 ± 5%, -40 ± 30%, and -53 ± 3%; p < 0.004). α-Adrenergic blockade had no effect on LAD cross-sectional area, while nicardipine partially reversed the ethanol-induced vasoconstriction. No significant change in vessel cross-sectional area took place in control dogs. These data suggest that ethanol induces epicardial coronary artery vasoconstriction in dogs at clinically important blood levels. α-Adrenergic blockade does not alter or reverse ethanol-induced vasoconstriction, while calcium channel blockade appears to be an effective vasodilator of ethanol-constricted vessels.