Chronic ingestion of low doses of ethanol protects the myocardium from isch
emic injury by activating adenosine receptors and protein kinase C. We test
ed the hypothesis that ATP-dependent potassium (K-ATP) channels mediate the
se beneficial effects. Dogs were fed with ethanol (1.5 g/kg) or water mixed
with dry food twice per day for 12 wk. After they were acutely instrumente
d for measurement of hemodynamics, dogs received saline (vehicle) or glybur
ide (0.1 mg/kg iv) and were subjected to 60 min of coronary artery occlusio
n followed by 3 h of reperfusion. Infarct size (through triphenyltetrazoliu
m chloride staining) was significantly (P < 0.05) reduced to 14 <plus/minus
> 1% of the left ventricular area at risk in ethanol-pretreated dogs compar
ed with controls (25 +/- 2%). Glyburide alone did not affect infarct size (
25 +/- 3%) but abolished the protective effects of ethanol pretreatment (28
+/- 3%). No differences in hemodynamics or coronary collateral blood flow
(through radioactive microspheres) were observed among groups. The results
indicate that K-ATP channels mediate the protective effects of chronic cons
umption of ethanol.