Abstract

As part of an ongoing study to evaluate the pathogenesis of neonatal hypoxic-ischemic brain injury, we have studied the effect of hypoxemia and severe hypotension on newborn brain metabolism. In 5 puppies, severe hypoxemia was produced by having the puppy breath a 4% O2/96% N2 mixture; normal MAP was maintained. In 7, severe hypotension (MAP 20-25 mmHg) was induced by hemorrhage; these animals spontaneously hyperventilated and maintained normal or elevated pO2. During these insults, local cerebral glucose utilization (LCGU) was studied using quantitative autoradiography and 14C-deoxyglucose. Hypoxemia caused a marked increase in LCGU to all brain structures: increases of 200-300% occurred diffusely in cerebral cortex and subcortical nuclei; increases of 300-600% occurred in white matter. Severe hypotension caused localized increases in LCGU: increases of 300-500% were seen in parasagittal cerebrum; increases of 150-200% were seen in the subependymal zone. The distribution of the increased LCGU correlated with the presumed distribution of pathologic injury after both insults; i.e. diffuse neuronal necrosis after hypoxemia and watershed infarction after severe hypotension. The increased LCGU probably represents a pathologic disruption of oxidative metabolism. The resultant increase in local tissue lactate may further injure brain elements locally. Thus, increased LOGU may be both a marker of the most vulnerable brain regions after insult and also an important step in the pathogenesis of neonatal hypoxic ischemic brain injury.

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