Hypoxic-ischemic cerebral necrosis in midgestational sheep fetuses: physiopathologic correlations.

Thirty-eight midgestational sheep fetuses were exposed 120 min to marked hypoxia. The brains in eight that reduced their mean arterial blood pressure to less than 30 mm Hg were markedly damaged. In these same fetuses the serum lactic acid concentrations were elevated during exposure to hypoxia to excessively high values (greater than 15 mM) and remained elevated for a prolonged period during recovery. Twenty-one fetuses exposed to the same magnitude of hypoxia that maintained their blood pressure unchanged showed less marked elevations of serum lactate concentrations and remained brain-intact. Greater quantities of pentobarbital administered to the ewes during hypoxia seemed to protect the brain from hypoxia and this effect was dose-dependent. Exposure of midgestational sheep fetuses to marked hypoxia associated with reductions in cerebral blood flow due to decreased blood pressure and impaired cerebral autoregulation caused major focal cerebral necrosis.