Cerebral oxidative metabolism during sustained hypoxaemia in fetal sheep.

Cerebral oxidative metabolism was determined in 9 unanaesthetized fetal sheep near term, during a normoxic control period and during sustained hypoxaemia induced by lowering maternal inspired O2 concentration to 11-8% with 3% CO2 added. Preductal arterial and sagittal vein blood samples were analyzed for oxygen content, blood gas tensions and pH. Cerebral blood flow was measured with a radioactively-labelled microsphere technique. Induced fetal hypoxaemia resulted in a metabolic acidaemia which was progressive over several h. Cerebral oxygen consumption was initially marginally decreased in response to induced hypoxaemia with cerebral blood flow increased thus maintaining O2 delivery coupled to cerebral oxygen consumption. With a worsening metabolic acidemia, pHa below 7.15, cerebral blood flow fell as mean arterial pressure fell, but cerebral oxygen consumption was little changed as fractional O2 extraction now increased. With sustained hypoxaemia and profound metabolic acidaemia, pHa below 7.00, fractional O2 extraction also fell resulting in a terminal fall in cerebral oxygen consumption to less than 50% of control values. Although the initial marginal decrease in cerebral oxygen consumption in response to induced hypoxia may represent a protective mechanism whereby the fetal brain decreases nonessential functions thus lowering oxidative needs, the terminal fall in cerebral oxygen consumption suggests pathological alterations within the brain at this time.