The depression of evoked cortical potentials caused by brief periods of cerebral ischemia is attenuated by prior intra- carotid injection of either ergotamine (2 or 6 μg) or dihydroergotoxin (6–20 μg). Studies in hypercapnic (hypoventilated) cats suggest that the protection afforded by ergot alkaloids is due to a metabolic effect rather than to a vasodilator effect.