Phospholipase C activation is required for cardioprotection by ethanol consumption

Regular alcohol consumption decreases the incidence of myocardial infarction (MI) and improves post-MI survival. It has previously been reported that chronic ethanol exposure induces long-term protection against cardiac ischemia/reperfusion injury, which improves myocardial recovery after MI. Chroni...

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Bibliographic Details
Published in:Experimental and clinical cardiology 2003, Vol.8 (4), p.184-188
Main Authors: Miyamae, Masami, Domae, Naochika, Zhou, Hui-Zhong, Sugioka, Shingo, Diamond, Ivan, Figueredo, Vincent M
Format: Article
Language:English
Subjects:
Experimental Cardiology
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Summary:Regular alcohol consumption decreases the incidence of myocardial infarction (MI) and improves post-MI survival. It has previously been reported that chronic ethanol exposure induces long-term protection against cardiac ischemia/reperfusion injury, which improves myocardial recovery after MI. Chronic cardioprotection by ethanol requires the activation of myocyte adenosine A1 receptors and sustained intramyocyte translocation of epsilon protein kinase C. A1 receptors activate phospholipase C (PLC). In the present paper, the role of PLC in mediating ethanol's protective effect against ischemia/reperfusion injury is investigated. Isolated hearts from guinea pigs fed 2.5% ethanol in their water for four months were subjected to ischemia/reperfusion. Hearts from ethanol-treated animals showed improved recovery of left ventricular developed pressure compared with controls (61% versus 38% of baseline, respectively; P
ISSN:1205-6626