Lidocaine accelerates recovery of brain electrical activity after 3 minutes of complete ischemia in the rabbit.
We recently reported that the continuous infusion of a low dose of lidocaine accelerated the recovery of the electroencephalogram and somatosensory evoked potentials after 20 min of incomplete cerebral ischemia in a single carotid artery preparation in the rabbit. In contrast, the recovery of the electroencephalogram and the auditory evoked potentials was minor on a comparable animal preparation subjected to 5 min of almost complete global ischemia. In the present study, we tested the hypothesis that the facilitatory effect of lidocaine on neuroelectrical recovery is of importance only during a certain combination of duration and severity of an ischemic episode. Similar to the previous studies, the rabbits had one carotid and both vertebral arteries permanently occluded and the other carotid artery reversibly clamped during the ischemic test. In the halothane-anesthetized animals, we monitored mean arterial pressure, carotid stump pressure, cerebral blood flow, auditory evoked potentials, and the electroencephalogram, before and for 90 min after 3 min of complete ischemia. The amplitude of the P1 wave (latency of 10 ms) of the auditory evoked potentials recovered more rapidly than on the previous 5 min preparation and returned towards the control amplitude more completely (p <0.05) in the lidocaine group. More importantly, the amplitude of the P2 wave (latency of 25 ms) recovered only 11% in the control group and 55% (p <0.05) in the lidocaine-infused animals. Comparable effects were observed in the early recovery of electroencephalographic activity during reperfusion. The present findings support the hypothesis that lidocaine may facilitate the recovery of the electroencephalogram and the evoked potentials only when an ischemic episode is below a certain combined level of duration and severity. The accelerating effect of lidocaine on postischemic neuroelectrical recovery was observed using a low dose of the drug, and it was not associated with changes in hemodynamic or cerebrovascular parameters or of blood composition. The latter suggests that the reported action may be related to some specific property of the local anesthetic action of lidocaine, such as blockade of axonal Na channels.
Sustch
G
G
Department of Anesthesiology and Physiology, University of California, Los Angeles, California, U.S.A.
Rubinstein
E H
EH