Iterative transient cerebral ischemic aggressions were produced by interrupting the blood flow in both common carotid arteries for 2 min in unanesthetized cats whose basilar artery has been permanently ligated. The influence of ischemia upon cerebral cortex was assessed by recording electrocortical activity (ECoG), indirect pyramidal tract response (I) and thalamic (nucleus ventralis posterior lateralis) evoked potentials induced by electrical stimulation of the contralateral forelimb. In control animals, the repetition of ischemic episodes delayed the recovery of the indirect pyramidal tract response, demonstrating an impairment of cortical excitability. Otherwise, cerebral ischemia induced an increase of thalamic-evoked responses. This phenomenon appears to result from the suppression of inhibitory corticofugal influence. The effects of dihydroergotoxine mesylate (DHET) upon these responses have been evaluated after intravenous administration (0.05, 0.3 and 0.6 mg/kg). DHET did not significantly modify the disappearance times of the ECoG and of the I cortico-pyramidal response or the recovery delay of the ECoG, but it improved the recovery time of I and inhibited the ischemic increase of the thalamic-evoked potential (0.3 and 0.6 mg/kg). These results suggest that DHET exerts a protective effect on the ischemic cerebral cortex in the experimental conditions used.