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Departments of 1 Medicine (Cardiology), 2 Neurology, and 3 Cellular and Molecular Pharmacology, and the 4 Ernest Gallo Clinic and Research Center, San Francisco General Hospital, University of California, San Francisco, California 94110
We recently discovered that regular alcohol
consumption reduces ischemia-reperfusion injury to the same
degree as ischemic preconditioning in guinea pig hearts. Ischemic
preconditioning, like this cardioprotective effect of alcohol, is
mediated by adenosine signaling in guinea pigs. In rats, ischemic
preconditioning may be mediated predominantly by
1-adrenergic signaling. To be
certain that this protective effect of alcohol is a general biological response, we searched for alcohol's cardioprotection in rat and identified a potential signaling mechanism. Hearts isolated from alcohol-fed guinea pigs and rats were subjected to
ischemia-reperfusion. Hearts from alcohol-fed animals showed
greater recovery of left ventricular developed pressure than controls
(guinea pigs, 46 vs. 29%; rats, 50 vs. 31%) and decreased myocyte
necrosis assessed by creatine kinase release (guinea pigs, 204 ± 42 vs. 440 ± 70 U · ml
1 · g
dry wt1; rats 158 ± 13 vs. 328 ± 31 U · ml1 · g
dry wt1). Adenosine
receptor blockade
[8-(p-sulfophenyl)theophylline] abolished alcohol's protection in guinea pig but not rat hearts. By
contrast, 1-adrenergic blockade
(prazosin) abolished alcohol's protection in rat but not guinea pig
hearts. We conclude that regular alcohol consumption reduces
ischemia-reperfusion injury and is mediated by species-specific
signaling mechanisms. A major goal of cardiovascular research is to
find a pharmacologically induced chronic state of preconditioning.
Understanding the mechanisms of alcohol's cardioprotection against
ischemia-reperfusion injury may aid in reaching this goal.
ethanol; preconditioning; adenosine; 1-adrenergic receptor; 8-(p-sulfophenyl)theophylline; prazosin
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