Oxidants, antioxidants, alcohol and stroke.

Free radicals are involved in the formation of both atherosclerosis and thrombosis. Therefore, considerable interest has recently been aroused by their role in the development of ischemic cerebral injury. Experimental observations suggest that antioxidants could reduce cerebral arterial vasospasm, reduce infarct size and prevent the development of both atherosclerosis and thrombosis. However, clinical evidence for these beneficial effects is still lacking. Alcohol can act as an antioxidant and an oxidant, and its intake seems to exert both beneficial and untoward effects on stroke, depending on drinking habits. Light-to-moderate regular alcohol intake has been suggested to protect against internal carotid artery atherosclerosis, a major cause of ischemic stroke. Ethanol metabolism in human blood vessel walls could antagonize the oxidation of LDL and thereby prevent the development of atherosclerosis. In addition, ethanol and the phenolic compounds of wine could decrease platelet aggregation and thromboxane formation and also prevent thrombus formation. Whether the effects are clinically significant remains to be proved. On the other hand, recent heavy drinking has been observed to worsen vasospastic ischemia caused by subarachnoid bleeding. Whether a lack of antioxidants is responsible for this effect also remains to be proved. Future stroke research should focus on solving these problems.