Lidocaine delays cortical ischemic depolarization: relationship to electrophysiologic recovery and neuropathology.
Academic Article
Overview
abstract
To determine if the previously reported limitation of i.v. lidocaine in facilitating recovery from cerebral ischemia was related to an effect on ischemic depolarization, we recorded cortical DC potential, electrocorticogram (ECoG) or EEG, and evoked potentials in rabbits subjected to either 3 or 5 min of complete ischemia. Three control animals undergoing 3 min of ischemia and all animals subjected to 5 min of ischemia were continuously monitored under anesthesia for 24 h, at which time the brains were processed for neocortical histology. Complete ischemia was produced by occlusion of the basilar artery and cervical collateral vessels followed by transient snare occlusion of the brachiocephalic trunk. In control animals of either ischemic duration, the onset of 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 195 +/- 15 s (n = 9) in lidocaine animals with 5 min ischemia (p < .01 and p < .0005 respectively, compared to controls of the same ischemic duration). In 3-min ischemia, lidocaine also reduced the amplitude of the 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 EEG duration and hastened the recovery of evoked potentials in animals with 3-min ischemia; with 5-min ischemia, however, there was no significant difference in the recovery of either type of electrical activity between control and lidocaine-treated animals. Significant correlations were found between the recovery of cortical electrical activity (both spontaneous and evoked) and the amplitude or integral of the ischemic depolarization shift (p < .001 in each case). Postischemic epileptiform bursts accompanied by negative DC shifts occurred in 3/7 controls and 4/7 lidocaine animals after reperfusion for > 12 h following 5-min ischemia. There was no significant difference in the degree of cortical neuronal injury or status spongiosus found between lidocaine and control animals subjected to 5-min ischemia and 24 h reperfusion. Cortical injury in control animals with 3-min ischemia was negligible and not significantly different from sham-operated animals.(ABSTRACT TRUNCATED AT 400 WORDS)
