Beneficial effects of low doses of ethanol on reoxygenation injury following anoxia in rat hearts

We investigated the effect of ethanol on adverse effects of anoxia and reoxygenation in isolated rat hearts. Perfusion of the anoxic Krebs-Henseleit medium for 40 min followed by 30 min of perfusion with aerobic medium produced considerable myocardial cell injury. Incorporation of ethanol (21.7 mM),...

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Published in:Basic research in cardiology 1989-07, Vol.84 (4), p.378-387
Main Authors: ASHRAF, M, MEYIAN RAHAMATHULLA, P
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - analysis
Animals
Biological and medical sciences
Calcium - analysis
Cardiovascular system
Coronary Disease - therapy
Creatine Kinase - analysis
Ethanol - pharmacology
Male
Medical sciences
Miscellaneous
Myocardial Reperfusion Injury - metabolism
Myocardial Reperfusion Injury - prevention & control
Pharmacology. Drug treatments
Rats
Rats, Inbred Strains
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container_title Basic research in cardiology
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creator ASHRAF, M
MEYIAN RAHAMATHULLA, P
description We investigated the effect of ethanol on adverse effects of anoxia and reoxygenation in isolated rat hearts. Perfusion of the anoxic Krebs-Henseleit medium for 40 min followed by 30 min of perfusion with aerobic medium produced considerable myocardial cell injury. Incorporation of ethanol (21.7 mM), in both anoxic and aerobic perfusion media resulted in a significant reduction of cell injury and inhibition of creatine phosphokinase release. The contraction bands were reduced to 0.24 as compared to 1.14 per field in the non-treated hearts. The tissue Ca++ was decreased to 8.72 mumol/gm/dry dry wt as compared to 20.17 mumol/gm/dry wt), as compared to the nontreated anoxic tissue (4.41 mumol/gm/dry wt). However, the inclusion of only ethanol in the anoxic medium did not decrease the damage, suggesting that maximal injury occurred during reoxygenation. Ethanol appears to inhibit myofibril contractures and preserve the structural integrity of plasma membrane during anoxia and reoxygenation. This study suggests a beneficial effect of ethanol in low doses on the post anoxic reperfusion injury in the myocardium.
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Perfusion of the anoxic Krebs-Henseleit medium for 40 min followed by 30 min of perfusion with aerobic medium produced considerable myocardial cell injury. Incorporation of ethanol (21.7 mM), in both anoxic and aerobic perfusion media resulted in a significant reduction of cell injury and inhibition of creatine phosphokinase release. The contraction bands were reduced to 0.24 as compared to 1.14 per field in the non-treated hearts. The tissue Ca++ was decreased to 8.72 mumol/gm/dry dry wt as compared to 20.17 mumol/gm/dry wt), as compared to the nontreated anoxic tissue (4.41 mumol/gm/dry wt). However, the inclusion of only ethanol in the anoxic medium did not decrease the damage, suggesting that maximal injury occurred during reoxygenation. Ethanol appears to inhibit myofibril contractures and preserve the structural integrity of plasma membrane during anoxia and reoxygenation. This study suggests a beneficial effect of ethanol in low doses on the post anoxic reperfusion injury in the myocardium.</description><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/BF02650872</identifier><identifier>PMID: 2818437</identifier><identifier>CODEN: BRCAB7</identifier><language>eng</language><publisher>Heidelberg: Springer</publisher><subject>Adenosine Triphosphate - analysis ; Animals ; Biological and medical sciences ; Calcium - analysis ; Cardiovascular system ; Coronary Disease - therapy ; Creatine Kinase - analysis ; Ethanol - pharmacology ; Male ; Medical sciences ; Miscellaneous ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - prevention &amp; control ; Pharmacology. 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Perfusion of the anoxic Krebs-Henseleit medium for 40 min followed by 30 min of perfusion with aerobic medium produced considerable myocardial cell injury. Incorporation of ethanol (21.7 mM), in both anoxic and aerobic perfusion media resulted in a significant reduction of cell injury and inhibition of creatine phosphokinase release. The contraction bands were reduced to 0.24 as compared to 1.14 per field in the non-treated hearts. The tissue Ca++ was decreased to 8.72 mumol/gm/dry dry wt as compared to 20.17 mumol/gm/dry wt), as compared to the nontreated anoxic tissue (4.41 mumol/gm/dry wt). However, the inclusion of only ethanol in the anoxic medium did not decrease the damage, suggesting that maximal injury occurred during reoxygenation. Ethanol appears to inhibit myofibril contractures and preserve the structural integrity of plasma membrane during anoxia and reoxygenation. This study suggests a beneficial effect of ethanol in low doses on the post anoxic reperfusion injury in the myocardium.</description><subject>Adenosine Triphosphate - analysis</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Calcium - analysis</subject><subject>Cardiovascular system</subject><subject>Coronary Disease - therapy</subject><subject>Creatine Kinase - analysis</subject><subject>Ethanol - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - prevention &amp; control</subject><subject>Pharmacology. 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Perfusion of the anoxic Krebs-Henseleit medium for 40 min followed by 30 min of perfusion with aerobic medium produced considerable myocardial cell injury. Incorporation of ethanol (21.7 mM), in both anoxic and aerobic perfusion media resulted in a significant reduction of cell injury and inhibition of creatine phosphokinase release. The contraction bands were reduced to 0.24 as compared to 1.14 per field in the non-treated hearts. The tissue Ca++ was decreased to 8.72 mumol/gm/dry dry wt as compared to 20.17 mumol/gm/dry wt), as compared to the nontreated anoxic tissue (4.41 mumol/gm/dry wt). However, the inclusion of only ethanol in the anoxic medium did not decrease the damage, suggesting that maximal injury occurred during reoxygenation. Ethanol appears to inhibit myofibril contractures and preserve the structural integrity of plasma membrane during anoxia and reoxygenation. 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source Springer Nature - Springer Journals Archive Collection
subjects Adenosine Triphosphate - analysis
Animals
Biological and medical sciences
Calcium - analysis
Cardiovascular system
Coronary Disease - therapy
Creatine Kinase - analysis
Ethanol - pharmacology
Male
Medical sciences
Miscellaneous
Myocardial Reperfusion Injury - metabolism
Myocardial Reperfusion Injury - prevention & control
Pharmacology. Drug treatments
Rats
Rats, Inbred Strains
title Beneficial effects of low doses of ethanol on reoxygenation injury following anoxia in rat hearts
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