Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs

Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O₂ consumption (CMR(O₂)) than in postnatal sheep. The fetus is exposed to a lower PO₂. We tested the hypothesis that low PO₂ in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMR(O₂). Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O₂ mixture to reduce arterial O₂ saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 ± 3 (SE) mmHg] and hypoxic (14 ± 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady- state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMR(O₂) were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO₂ is unlikely to be the major mechanism for the potent Cushing response in the fetus.