LIDOCAINE DELAYS CORTICAL ISCHEMIC DEPOLARIZATION - RELATIONSHIP TO ELECTROPHYSIOLOGIC RECOVERY AND NEUROPATHOLOGY

To determine if the previously reported limitation of i.v. lidocaine i n facilitating recovery from cerebral ischemia was related to an effec t on ischemic depolarization, we recorded cortical DC potential, elect rocorticogram (ECoG) or EEG, and evoked potentials in rabbits subjecte d to either 3 or 5 min of complete ischemia. Three control animals und ergoing 3 min of ischemia and all animals subjected to 5 min of ischem ia were continuously monitored under anesthesia for 24 h, at which tim e the brains were processed for neocortical histology. Complete ischem ia was produced by occlusion of the basilar artery and cervical collat eral vessels followed by transient snare occlusion of the brachiocepha lic trunk. In control animals of either ischemic duration, the onset o f ischemic depolarization occurred at 102 +/- 5 s (n = 18). In animals receiving 0.2 mg/kg/min lidocaine infusion, the negative DC shift was delayed to 182 +/- 28 s (n = 7) in animals with 3-min ischemia and 19 5 +/- 15 s (n = 9) in lidocaine animals with 5 min ischemia (p < .01 a nd p < .0005 respectively, compared to controls of the same ischemic d uration). In 3-min ischemia, lidocaine also reduced the amplitude of t he DC shift from 8.9 +/- 0.4 mV to 4.6 +/- 1.1 mV (p < .005), whereas in 5-min ischemia there was no significant difference in the amplitude of the shift between lidocaine and control animals (11.1 +/- 1.4 and 12.7 +/- 1.0 mV, respectively). Lidocaine shortened the isoelectric EE G duration and hastened the recovery of evoked potentials in animals w ith 3-min ischemia; with 5-min ischemia, however, there was no signifi cant difference in the recovery of either type of electrical activity between control and lidocaine-treated animals. Significant correlation s were found between the recovery of cortical electrical activity (bot h spontaneous and evoked) and the amplitude or integral of the ischemi c depolarization shift (p < .001 in each case). Positischemic epilepti form bursts accompanied by negative DC shifts occurred in 3/7 controls and 4/7 lidocaine animals after reperfusion for > 12 h following 5-mi n ischemia. There was no significant difference in the degree of corti cal neuronal injury or status spongiosus found between lidocaine and c ontrol animals subjected to 5-min ischemia and 24 h reperfusion. Corti cal injury in control animals with 3-min ischemia was negligible and n ot significantly different from sham-operated animals. We conclude tha t in this preparation, the delay in ischemic depolarization caused by lidocaine does not significantly alter the reversibility of the insult unless the ischemic duration is short enough to attenuate the shift d uring recirculation. However, such brief ischemic durations may not be of great enough severity to produce neuronal damage.