K(ATP) channels mediate the beneficial effects of chronic ethanol ingestion

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 (K(ATP)) channels mediate these beneficial effects. Dogs were fed with ethanol (1.5 g/kg) or water mixe...

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Published in:American journal of physiology. Heart and circulatory physiology 2000-11, Vol.279 (5), p.H2574-H2579
Main Authors: Pagel, P S, Toller, W G, Gross, E R, Gare, M, Kersten, J R, Warltier, D C
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Administration, Oral
Animals
Collateral Circulation - drug effects
Collateral Circulation - physiology
Coronary Circulation - drug effects
Coronary Circulation - physiology
Dogs
Drug Administration Schedule
Ethanol - administration & dosage
Glyburide - pharmacology
Heart - drug effects
Heart - physiology
Hemodynamics - drug effects
Myocardial Infarction - metabolism
Myocardial Infarction - pathology
Myocardial Infarction - prevention & control
Potassium Channels - metabolism
Protein Kinase C - metabolism
Receptors, Purinergic P1 - metabolism
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Summary: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 (K(ATP)) 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 K(ATP) channels mediate the protective effects of chronic consumption of ethanol.
ISSN:0363-6135
DOI:10.1152/ajpheart.2000.279.5.h2574