Cerebral metabolic activity was measured in ten dogs undergoing deep hypothermia and circulatory arrest for 45 minutes using a method of surface induced cooling, ether anesthesia, and hyperventilation. Cerebral blood flow and cerebral oxygen consumption were measured utilizing a mass spectrometer by the inert gas technic. Cerebral oxygen consumption at the completion of circulatory arrest and rewarming increased 15% over the mean pre cooling rate of oxygen consumption, indicating a restoration of adequate cerebral metabolic activity. A mean decrease in the cerebral blood flow of 18% and an increase of cerebral vascular resistance of 8% in the post arrest state was found, suggesting mild cerebral vascular damage. Direct and continuous measurements of the cerebral cortical PCO2 and PCO2 levels during the 45 minutes of circulatory arrest in five animals indicate continuing cerebral metabolic activity during the arrest period, with brain oxygen utilization ceasing after the first 15 minutes of the arrest period. Despite the marked lowering of the blood PCO2 levels in the animals at deep hypothermic levels as a result of the hyperventilation, there was no evidence of an increase in cerebral vascular resistance. Using the technic of surface induced hypothermia with ether anesthesia and hyperventilation, circulatory arrest for 45 minutes at 18 C was tolerated by the animals without evidence of impairment of cerebral metabolism, despite a consistent reduction in cerebral blood flow.
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