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 expose d to a lower PO2. We tested the hypothesis that low PO2 in postnatal l ambs potentiates peripheral vasoconstriction and better maintains cere bral perfusion pressure and CMR(O2). Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O 2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation o f intracranial pressure to within 3-5 mmHg of baseline mean arterial p ressure for 30 min by ventricular fluid infusion initially caused a si milar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmH g] 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 f urther with elevated intracranial pressure. Moreover, there was no sig nificant difference between groups in the steady-state increase in art erial pressure, and microsphere-determined blood flow to intestines, k idney, skin, and muscle did not decrease in either group. Consequently , cerebral perfusion pressure, regional cerebral blood flow, and CMR(O 2) were reduced similarly in both groups. Therefore, hypoxemia-failed to potentiate the postnatal pressor response. Low PO2 is unlikely to b e the major mechanism for the potent Cushing response in the fetus.