In the present experiments, we tested the effect of a continuous infusion of low-dose lidocaine on the time course of neuroelectrical recovery after an episode of almost complete ischemia in our single carotid artery model in the rabbit. In this preparation, carotid clamping elicited suppression of the electroencephalogram in less than 15 s, a drop in carotid stump pressure below 15 mm Hg, and evidence of minimal cerebral collateral perfusion in postortem studies. We monitored mean arterial pressure, cerebral blood flow, carotid stump pressure, electroencephalogram, and auditory evoked potentials during three periods: control (30 min), ischemia (5 min), and reperfusion (90 min). Low-dose lidocaine (0.05 mg/kg/min) was continuously infused throughout the three periods. We specifically measured two peaks of the auditory evoked potentials and the most important finding was that the early wave (P1) partially recovered: to 35-40% in the control and to 64% in the lidocaine group (p < 0.05 after 90 min). In contrast, the recovery of the later water wave (P2) was very incomplete in both groups, and reached only 25-30% of the control amplitude. Similarly, the electroencephalogram of all of the rabbits failed to return to the control pattern but more animals in the lidocaine group (p < 0.05) showed fewer pathological waves at the end of reperfusion. The present results indicate that a low dose of lidocaine had a small but significant action on electrical recovery after brief, almost complete global ischemia, confirming our previous observations on a rabbit model where the ischemic episode was less severe and the recovery more complete. These findings suggest that a low dose of lidocaine can accelerate the time course of neuroelectrical recovery after global ischemia and that the magnitude of this action depends very critically on the duration and severity of the ischemic event.