Calcium entry blockers can ameliorate postischemic cerebral hypoperfusion, protect the myocardium against
ischemia, and may protect against early postischemic
neurologic deficit. This study documents that a
calcium entry blocker, given after
cardiac arrest, can ameliorate late postischemic
neurologic deficit (ND). Thirty-four dogs received 10 min of
ventricular fibrillation, restoration of spontaneous circulation by external
cardiopulmonary resuscitation, and standard postarrest
intensive care. Eleven of these dogs were given
lidoflazine, 1 mg/kg
body weight, within 10 min postarrest and again at 8 h and 16 h. Pupillary light reflexes, EEG activity, arterial-cerebrovenous
oxygen gradients (O2 demand/supply ratios) and intracranial pressure were the same in both groups. After weaning from controlled ventilation at 24 h, ND scores improved consistently through the 96-h observation period in the
lidoflazine-treated dogs. In the control group, ND scores were significantly higher than in the
lidoflazine-treated dogs. In the
lidoflazine-treated group, 5/11 dogs achieved normal overall performance and none remained
comatose, whereas all control dogs had some deficit and 4/11 remained
comatose. Delayed neurologic deterioration occurred in 6/11 control and 0/11
lidoflazine-treated dogs. Total mean cerebral histopathologic damage (HD) scores at 96 h were not significantly different between the two groups; however, individual HD scores and maximum cerebro-spinal fluid (brain-specific)
creatine-phosphokinase activity--which increases after brain insults--correlated well with 96-h ND scores. In the
lidoflazine group, life-threatening dysrhythmias were less frequent and the
norepinephrine requirement for blood pressure maintenance was the same as in the control group. Cardiac output remained at prearrest levels in the
lidoflazine-treated dogs, but decreased in the control group, particularly during the first 4 h postarrest.