Moderate use of alcohol has shown protective effects in
coronary artery disease, while excessive use has been associated with
cardiomyopathy and
hypertension. Since alcohol is a
vasodilator, we postulated that it might have protective effects when administered acutely in the setting of
ischemia/reperfusion. Therefore, we studied the acute effects of alcohol on
myocardial infarction in a rabbit model. Anesthetized, open chest rabbits were subjected to a 30 minute coronary artery occlusion followed by 4 hours of reperfusion. Rabbits were randomized to a control group (n = 20), receiving an infusion of 10 ml
normal saline, intravenously, over 10 minutes via a Harvard pump, or an alcohol group (n = 20), receiving a diluted
solution of 100%
ethanol (1 ml/kg diluted in
normal saline to 10 ml total
solution) infused in a similar fashion. This infusion regimen resulted in an average
blood alcohol level of 110 mg/dl (range 77-129) tested in five rabbits within the study. Ten minutes after in fusion, a marginal branch of the circumflex artery was occluded. Regional myocardial blood flow during
coronary occlusion and reperfusion was measured using radioactive
microspheres. Myocardial ischemic area at risk (AR) was assessed by blue
dye injection and myocardial
necrosis (AN) by
triphenyltetrazolium chloride (TTC) staining. The mean regional coronary blood flow in ischemic tissue was 0.04 +/- 0.01 ml/min/g in the control group versus 0.03 +/- 0.01 ml/min/g in the experimental group (p = NS) and averaged 1.74 ml/min/g (control) to 1.98 ml/min/g (alcohol) in the nonischemic tissue. All rabbits received comparable ischemic insult: Collateral blood flow and AR were similar in both groups. An overall analysis showed no significant reduction in
infarct size (expressed as the percent of necrotic tissue within the area at risk) in the alcohol group (23 +/- 3%) compared with the control group (27 +/- 4%). In conclusion, alcohol did not reduce
infarct size in the rabb it model.