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Alcohol and Alcoholism Vol. 38, No. 1, pp. 18-24, 2003
© 2003 Medical Council on Alcohol

CHRONIC ETHANOL CONSUMPTION MODULATES MYOCARDIAL ISCHAEMIA–REPERFUSION INJURY IN MURINE AIDS

Yinhong Chen1,2, Grace Davis-Gorman2, Ronald R. Watson1,* and Paul F. McDonagh2

1 Division of Health Promotion Science, College of Public Health and
2 Cardiovascular and Thoracic Surgery and The Sarver Heart Center, School of Medicine, University of Arizona, Tucson, AZ 85724, USA

Received 23 November 2001; first review notified 17 July 2002; accepted 30 July 2002

— Aims: The severity of cardiovascular complications in acquired immune deficiency syndrome (AIDS) patients may be associated with acute ischaemia–reperfusion injury. Epidemiological studies suggest that moderate ethanol consumption has myocardial protective effects. However, it is unknown if chronic ethanol consumption benefits acute myocardial ischaemia–reperfusion injury in AIDS. The aim of this study was to determine if chronic ethanol consumption modulates myocardial ischaemia–reperfusion injury in murine AIDS. Methods: Four groups were studied: control, murine AIDS, ethanol, and ethanol plus murine AIDS. All mice were subjected to 30 min of left anterior descending branch (LAD) occlusion and 120 min of reperfusion. Results: We found that the survival from an acute myocardial infarction was reduced in advanced-stage murine AIDS mice. Although early-stage murine AIDS hearts did survive in acute myocardial infarction, the infarct size was significantly larger. Chronic ethanol consumption significantly decreased infarct size compared to the control group. Chronic ethanol consumption also improved the survival of murine AIDS mice from an acute myocardial infarction. However, chronic ethanol consumption did not significantly reduce infarct size in murine AIDS. Conclusions: Our results indicate that multiple deleterious effects may enhance acute ischaemia–reperfusion injury in murine AIDS. The beneficial effects of chronic ethanol consumption in myocardial ischaemia–reperfusion injury may be due to modulation of neutrophil adhesion molecule expression and cytokine secretion.


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