K(ATP) channels mediate the beneficial effects of chronic ethanol ingestion. Am J Physiol Heart Circ Physiol 2000 Nov;279(5):H2574-9
Date
10/25/2000Pubmed ID
11045996DOI
10.1152/ajpheart.2000.279.5.H2574Scopus ID
2-s2.0-0033672339 (requires institutional sign-in at Scopus site) 39 CitationsAbstract
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.
Author List
Pagel PS, Toller WG, Gross ER, Gare M, Kersten JR, Warltier DCMESH terms used to index this publication - Major topics in bold
Adenosine TriphosphateAdministration, Oral
Animals
Collateral Circulation
Coronary Circulation
Dogs
Drug Administration Schedule
Ethanol
Glyburide
Heart
Hemodynamics
Myocardial Infarction
Potassium Channels
Protein Kinase C
Receptors, Purinergic P1
