Acute Alcohol-induced Protection against Infarction in Rabbit Hearts: Differences from and Similarities to Ischemic Preconditioning

Recent studies reveal that brief ethanol exposure induces cardioprotection against simulated ischemia in cardiomyocytes by the activation of protein kinase C- ϵ. The present study tests the ability of ethanol to induce protection in rabbit hearts in which infarct size was the end-point and explores...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology 2001-11, Vol.33 (11), p.2015-2022
Main Authors: Krenz, Maike, Baines, Christopher P., Heusch, Gerd, Downey, James M., Cohen, Michael V.
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Alcohols - pharmacology
Alkaloids
Analysis of Variance
Animals
Anti-Arrhythmia Agents - pharmacology
Benzophenanthridines
Decanoic Acids - pharmacology
Enzyme Activation
Enzyme Inhibitors - pharmacology
Ethanol
Ethanol - pharmacology
Genistein - pharmacology
Glyburide - pharmacology
Heart - drug effects
Heart - physiology
Hemodynamics
Hydroxy Acids - pharmacology
Ischemic preconditioning
Ischemic Preconditioning, Myocardial
Isoenzymes - metabolism
Myocardial Infarction - prevention & control
Myocardium - metabolism
Phenanthridines - pharmacology
Potassium Channels - metabolism
Protein kinase C
Protein Kinase C - antagonists & inhibitors
Protein Kinase C - metabolism
Protein Kinase C-epsilon
Rabbits
Rats
Signal Transduction
Time Factors
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Summary:Recent studies reveal that brief ethanol exposure induces cardioprotection against simulated ischemia in cardiomyocytes by the activation of protein kinase C- ϵ. The present study tests the ability of ethanol to induce protection in rabbit hearts in which infarct size was the end-point and explores the signal transduction pathways involved. In isolated rabbit hearts, 50 m m ethanol infused for 5 min with 10 min of washout prior to 30 min of regional ischemia reduced infarct size (triphenyltetrazolium chloride staining) by 49%. Neither adenosine receptor blockade with 8-(p -sulfophenyl) theophylline nor the free radical scavenger N-2-mercaptopropionyl glycine inhibited the protection triggered by ethanol. In contrast, protein kinase C inhibition with chelerythrine, protein tyrosine kinase inhibition with genistein, and blockade of ATP-sensitive potassium channels (KATP) with either 5-hydroxydecanoate or glibenclamide did abolish protection. Thus, transient ethanol exposure followed by washout prior to ischemia elicits a preconditioning-like effect involving protein kinase C, at least one protein tyrosine kinase, and KATPchannels, but neither adenosine nor free radicals.
ISSN:0022-2828
1095-8584
DOI:10.1006/jmcc.2001.1465