Chronic Alcohol Consumption Increases Infarct Size Following Transient Focal Cerebral Ischemia

Abstract

We examined the influence of chronic alcohol consumption on transient focal ischemia-induced brain damage. Sprague-Dawley rats were randomly divided into two groups, a control group and an alcohol group. Eight weeks after being fed a liquid diet with or without alcohol, rats were subjected to 2 hours of right middle cerebral artery occlusion (MCAO). Regional cerebral blood flow (rCBF) was monitored through a Laser-Doppler flow probe attached to the lateral aspect of the skull. Mortality rates, neurological evaluation, and infarct volume were assessed 24 hours after reperfusion. In separate experiments, response of parietal pial arterioles to hypoxia was measured using a cranial window technique. Compared to control, the mortality rate was significantly higher in alcohol-fed rats. In addition, alcohol-fed rats had significantly larger infarct volumes and worse neurological outcomes than rats in the control group. Furthermore, rCBF measurement indicated that the alcohol group had less rCBF regulatory capability than the control group during ischemia. Dilation of pial arterioles in response to hypoxia was significant reduced in the alcohol group. Our findings suggest that chronic alcohol consumption exacerbates transient focal ischemia-induced brain damage. We suggest that increased ischemic brain damage during alcohol consumption may be related to an impaired rCBF regulatory capability during ischemia.