Abstract
1. The effects of hypoxia and asphyxia on cerebral blood flow and oxidative metabolism have been investigated in the calf and lamb under sodium pentobarbitone anaesthesia. 2. Cerebral blood flow was determined using a hydrogen clearance technique, and cerebral metabolism quantified by the simultaneous measurement of arteriocerebral venous concentration differences for oxygen, glucose and lactate. Continuous measurements were made of arterial and cerebral venous PO2 in vivo. 3. Both cerebral blood flow and oxygen consumption were less in animals anaesthetized with sodium pentobarbitone than in conscious animals. 4. In the calf, recovery from transient episodes of severe hypoxia and asphyxia was associated with a rapid recovery and overshoot of cerebral venous PO2. Evidence was obtained that rapid changes in blood pressure during severe asphyxia were associated with pressure-passive cerebral blood flow. Prolonged hypoxia (Pa,O2:21 +/- 2 mmHg) with normocapnia was associated with an increase in cerebral blood flow, fall in cerebral oxygen consumption, and no change in the glucose-oxygen index. 5. In the lamb, prolonged asphyxia (Pa,O2:30 +/- 1 mmHg; Pa,CO2:56 +/- 2 mmHg) was associated with an increase in cerebral blood flow. Cerebral glucose uptake did not change, but cerebral oxygen consumption was markedly depressed, and the glucose-oxygen index increased. 6. In the lamb during normoxia, there was a linear correlation between cerebral blood flow and arterial PCO2 in the range 10-95 mmHg (r = 0.92; P < 0.001), with a slope of 1.74 ml. 100g-1 min-1 . mmHg Pa,CO2-1 . Hypoxia did not significantly increase the fall in cerebral vascular resistance associated with a rise in Pa,CO2 from 34 to 56 mmHg.