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Effects of Chronic Moderate and Heavy Ethanol Consumption on Myocardial Recovery from Ischemia
Author(s) -
Gibson Brian T.,
Ong Joseph H.,
Starnes Joseph W.,
Farrar Roger P.
Publication year - 1998
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1998.tb05920.x
Subject(s) - ischemia , creatine , medicine , ethanol , reperfusion injury , cardiology , calorie , diastole , hemodynamics , anesthesia , endocrinology , chemistry , biochemistry , blood pressure
The purpose of this study was to determine the effects of chronic moderate and heavy ethanol consumption on myocardial ischemia/reperfusion injury. Three groups (n = 18) of 6‐month‐old female Sprague‐Dawley rats were fed a nutritionally balanced liquid diet. Control, moderate alcohol, and heavy alcohol groups consumed 0%, 20%, and 35% of their calories from ethanol, respectively. After 10 weeks of feeding, hearts were isolated and subjected to 21.5 min of ischemia alone, or 21.5 min of ischemia followed by 30 min reperfusion. Hearts were evaluated for hemodynamic characteristics and high‐energy phosphate content. Hearts from animals exposed to moderate and heavy amounts of ethanol recovered significantly less (30.61% and 29.45%, respectively) of their preischemic cardiac external work than control hearts (65.52%). Postischemic diastolic stiffness was increased ˜7‐fold, and high‐energy phosphate content, both creatine phosphate and adenosine triphosphate, decreased >25% by both chronic moderate and heavy ethanol consumption. In conclusion, both chronic moderate and heavy ethanol consumption exacerbate myocardial ischemia/reperfusion injury. The ethanol‐induced reduction in postischemic energy status may be the mechanism of increased diastolic stiffness and subsequent reduced cardiac external work.