Inasmuch as ethanol is thought to exert its major effects on the CNS, it is important to determine whether this abused substance can exert any direct action on cerebral blood vessels. Since chronic ingestion of alcohol: (1) can produce a loss (and degeneration) of neurons and glial cells in the brain, and (2) is associated, often, with hallucinations in human subjects particularly those undergoing withdrawal, it is possible that ethanol could produce hypoxia in select regions of the brain. The available indirect evidence in man and animals, albeit equivocal, does indicate that ethanol in certain concentrations might produce deficits in cerebral blood flow in select regions of the brain. Direct in-situ observations on the rat brain, using high-resolution, quantitative TV image-intensification microscopy, indicates that administration of ethanol, irrespective of the route of administration (e.g., perivascularly, intraarterially or systemically), produces graded concentration-dependent spasms of arterioles and venules. Concentrations of ethanol approximately greater than 250 mg/dl produce intense spasms resulting in rupture of these vessels. Recent in-situ studies in conscious dogs, using radiolabelled microspheres, also indicate that ethanol can produce deficits in regional brain blood flow. Studies with isolated canine middle cerebral and basilar arteries clearly demonstrate that low concentrations of ethanol (e.g., (less than 10 mM) can produce concentration-dependent spasms by a direct vascular action. Collectively, these new findings could be used to support the concept that heavy use of alcohol or binge-drinking can produce stroke-like effects. Specific calcium antagonists prevented or reversed the alcohol-induced cerebrovasospasms in rats and may prove valuable in treating the hypertension and strokes observed in heavy users of alcohol.