M. Ayad et al., LIDOCAINE DELAYS CORTICAL ISCHEMIC DEPOLARIZATION - RELATIONSHIP TO ELECTROPHYSIOLOGIC RECOVERY AND NEUROPATHOLOGY, Journal of neurosurgical anesthesiology, 6(2), 1994, pp. 98-110
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.