Cats were subjected to circulatory arrest of 5 minutes duration by occlusion of the ascending aorta and the superior and inferior venae cavae. After perfusion was re-established by release of the occluding clamps, one group of animals was placed in a hyperbaric chamber and ventilated with oxygen at 1.5 atmospheres absolute pressure for 2.5 hours. Control animals were ventilated with oxygen at ambient atmospheric pressure. The time for electroencephalographic recovery was significantly shortened (P = 0.002) and the cerebrospinal fluid lactate change (2.5-hour value minus the preclamp value) was reduced (P = 0.008) in the animals receiving hyperbaric oxygen. The data indicate that hyperbaric oxygen administered after global cerebral ischemia modifies favorably both postischemic functional impairment and metabolic derangement. Possible mechanisms for the modification of postischemic encephalopathy are discussed.
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Kapp et al. (1982) studied this question.
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