Abstract

A 10-minute cardiac arrest was produced in dogs by electrical fibrillation of the heart. Recovery of cerebral function was monitored by estimating the cerebral metabolic rate of oxygen consumption (CMRO₂), cerebral blood flow (CBF), electroencephalograph (EEG) and extent of neurological deficit. The study group received flunarizine (0.1 mg/kg intravenously) at the beginning of resuscitation, while control animals were given the drug vehicle. By four hours after resuscitation, CMRO₂ in flunarizine-treated dogs was 121 ± 43% of pre-arrest baseline, as compared with 37 ± 9% in control animals (P < 0.02). In the flunarizine group, CBF was 83 ± 21% of baseline, while it was only 31 ± 8% in controls (P < 0.01). As compared with the control group, no other significant changes were detected in electrocardiographic, hemodynamic, or biochemical parameters in the flunarizine-treated dogs. A significant improvement in the visual EEG score (P < 0.001) and neurological deficit (P < 0.05) was seen in flunarizine-treated dogs six hours after ischemic insult.