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1 Division of Cardiovascular Diseases, Department of Medicine and 2 Departments of Anesthesiology and 3 Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee 53226; The Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin 53295 and 4 Department of Anesthesiology, University of Graz, Graz, Austria
Chronic ingestion of low doses of ethanol protects the myocardium from ischemic injury by activating adenosine receptors and protein kinase C. We tested the hypothesis that ATP-dependent potassium (KATP) channels mediate these 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 instrumented for measurement of hemodynamics, dogs received saline (vehicle) or glyburide (0.1 mg/kg iv) and were subjected to 60 min of coronary artery occlusion followed by 3 h of reperfusion. Infarct size (through triphenyltetrazolium chloride staining) was significantly (P < 0.05) reduced to 14 ± 1% of the left ventricular area at risk in ethanol-pretreated dogs compared 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 KATP channels mediate the protective effects of chronic consumption of ethanol.
myocardial infarction; infarct size; prolonged coronary occlusion; myocardial ischemia
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