Calcium Blockers in Cerebral Resuscitation

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Abstract
Recent studies on cerebral resuscitation following an ischemic anoxic insult suggest that both inadequate reperfusion and direct neuronal death are partially initiated by Ca2+ entry into vascular smooth muscle and neurons. To investigate the effects of Ca2+ blocking agents on cerebral resuscitation, a controlled perfusion arrest model with cardiopulmonary bypass was used. Post-resuscitation regional cerebral cortical blood flow (rCCBF) and intracranial pressures (ICP) were monitored in 5 control dogs and in 12 study dogs resuscitated after a prolonged (20 min) cardiac arrest. The resuscitation included dexamethasone and 3 agents thought to be Ca2+ entry antagonists and to offer potential cerebral protection after complete prolonged cerebral ischemic anoxia. Prearrest rCCBF measured by a thermal dilution method with a thermistor placed on the cerebral cortex was 2.0 .+-. 0.6 ml/min on bypass at 100 mm Hg mean arterial pressure. Twenty min after resuscitation was begun, the rCCBF in ml/min per were: controls 1.1 .+-. 0.3; dexamethasone (2 mg/kg) 1.2 .+-. 0.4; MgSO4 (100 mg/kg) 1.8 .+-. 0.5; verapamil (0.15 mg/kg) 1.9 .+-. 0.4 and lidoflazine (1 mg/kg) 1.5 .+-. 0.3. Ninety min following the beginning of resuscitation the rCCBF were: controls 0.1 .+-. 0.1; dexamethsone 0.1 .+-. 0.1; MgSO4, 1.7 .+-. 0.3; verapamil, 1.9 .+-. 0.4 and lidoflazine, 1.5 .+-. 0.3 ml/g per min. Ca2+ entry antagonists maintained cerebral blood flow at 20 and 90 min following prolonged ischemic anoxic insult. Dexamethasone was no better than control. Evidently Ca2+ entry blockers can maintain rCCBF and may have a significant role in cerebral resuscitation following cardiac arrest.