Cerebral blood flow and oxidative metabolism during hypoxia and asphyxia in the new‐born calf and lamb.

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Abstract
The effects of hypoxia and asphyxia on cerebral blood flow and oxidative metabolism were investigated in the calf and lamb under sodium pentobarbitone anesthesia. Cerebral blood flow was determined using a Hy clearance technique: cerebral metabolism was quantified by the simultaneous measurement of arteriocerebral venous concentration differences for O2, glucose and lactate. Continuous measurements were made of arterial and cerebral venous P[partial pressure]O2 in vivo. Cerebral blood flow and O2 consumption were less in animals anesthetized with sodium pentobarbitone than in conscious animals. 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[arterial], O2: 21 .+-. 2 mmHg) with normocapnia was associated with an increase in cerebral blood flow, fall in cerebral O2 consumption and no change in the glucose O2 index. 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 O2 consumption was markedly depressed, and the glucose-O2 index increased. 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 per min per mmHg Pa,CO2. Hypoxia did not significantly increase the fall in cerebral vascular resistance associated with a rise in Pa,CO2 from 34 to 56 mmHg.