Early amelioration of neurologic deficit by lidoflazine after fifteen minutes of cardiopulmonary arrest in dogs.

A prospective, controlled, blind study was done to test the effect of a calcium entry blocker on the neurologic integrity of dogs after cardiopulmonary arrest. Ten male mongrel dogs were anesthetized, prepared with sterile technique, and instrumented for pulmonary arterial (PA) and systematic arterial pressure monitoring. A left thoracotomy and pericardotomy were performed. Cardiac arrest was produced by injecting KCl (1 mEq/kg) through the PA line, and the respirator was stopped. Full arrest was maintained for 15 minutes. Thereafter, the dogs were resuscitated with ventilation, internal massage, fluids, bicarbonate, epinephrine, and internal defibrillation. All dogs were resuscitated within 6 to 10 minutes. Five control dogs received saline placebo, and five dogs were treated with lidoflazine (1 mg/kg) IV drip immediately post resuscitation. All dogs were scored neurologically every two hours by a deficit grading scale. All treated dogs had spontaneous ventilation, reactive pupils and corneals, voluntary movements, and responses to tactile stimulation at 12 hours post resuscitation. Four of five control dogs had maximum deficit scores without improvement. The difference in neurologic scores between the treated and control groups became increasingly divergent with time, and was statistically significant (P less than .05) by four hours post resuscitation. Thus the calcium antagonist lidoflazine produces improvement in neurologic recovery in the first 12 hours after cardiopulmonary arrest in dogs.