CEREBRAL BLOOD-FLOW AND OXIDATIVE BRAIN METABOLISM DURING AND AFTER MODERATE AND PROFOUND ARTERIAL HYPOXEMIA

In anesthetized artificially ventilated dogs the effect of graded arterial hypoxemia on cerebral blood flow (CBF) and on the oxidative carbohydrate metabolism of the brain was tested. The hypoxic vasodilatory influence on cerebral vessels was present even at moderate systemic hypoxemia, provided that PaCO2 [arterial tension of CO2] was kept within normal limits. At PaO2 of about 50 Torr, CBF increased from 56.6-89.7 ml/100 g per min. With increasing cerebral hyperemia (CBF increased to 110.9 ml/100 g per min, at PaO2 of 30 Torr), CMRO2 [cerebral metabolic rate of O2] (4.2 ml/100 g per min) was not significantly raised above its normal level (4.7 ml/100 g per min), even with profound arterial hypoxemia. This showed that CMRO2 levels were poor indices of hypoxic hypoxia. A disproportionately high increase in cerebral glucose uptake (CMR glucose levels rose from 4.4-10.4 mg/100 g per min) and enhanced cerebral glycolysis (CMR lactate changed from 0.2-1.6 mg/100 g per min) at moderately reduced PaO2 (50 Torr) indicated early metabolic changes, which became more marked with further falls in PaO2. Sixty minutes after restoration of a normal PaO2 level, CBF and brain metabolism were completely recovered. A short period of profound systemic hypoxemia apparently does not produce long lasting metabolic and circulatory disorders of the brain, provided the cerebral perfusion pressure does not vary and is kept at normal levels.