Summary:The effect of hypoxemia and cephalic hy potension, alone and in combination, on hemispherical CBF and metabolism was examined in seven chronically catheterized fetal sheep. Hypoxemia was induced by low ering the maternal inspired oxygen fraction and cephalic hypotension was generated by partial occlusion of the fetal brachiocephalic artery. CBF was measured with ra dionuclide-labeled microspheres. During control, the ar terial blood oxygen content (Cao2) was 3.2 ± 1.0 (SO) mM and CBF averaged 131 ± 21 (SO) ml min -I 100 g -I.The cephalic perfusion pressure (PP, mean cephalic arte rial -sagittal venous) was 40 ± 4 mm Hg and cerebral vascular resistance (CVR, PP/CBF) was 0.31 ± 0.06 mm Hg ml-I min 100 g. During induced hypoxemia, Cao2 was 1.4 ± 0.7 mM and CBF was elevated to 223 ± 60 ml min -I 100 g -I. PP was not different from control and CVR was lower at 0.19 ± 0.04 mm Hg ml-I min 100 g, reflecting cerebral vasodilation. With cephalic hypoten sion alone (PP = 21 ± 4 mm Hg; Ca�? = 3.4 ± 0.9 mM), CBF fell to 83 ± 23 ml min -I 100 g--I and there was no significant change in CVR (0.26 ± 0.05 mm Hg ml-I min It has long been appreciated that fetal cerebral vasodilation and the subsequent increase in blood flow is a very important protective response to hypoxemia (Jones et aI. , 1977(Jones et aI. , , 1978. However, when the fetus becomes severely hypoxemic, the arterial blood pressure may not be maintained and the brain must also endure hypotension (Wagner et aI., 1986). Concomitant hypoxemia and hypoten- Abbreviations used: Cao2, arterial blood oxygen content; Csvo2, sagittal venous blood oxygen content; CVR, cerebral vascular resistance; 00, oxygen delivery; PP, perfusion pres sure.99 100 g). During combined hypoxemia and hypotension (Cao2 = 1.5 ± 0.8 mM and PP = 18 ± 4 mm Hg), CBF was significantly greater than during hypotension alone (l00 ± 6 ml min-I 100 g). CVR was 0. 19 ± 0.05 mm Hg ml-I min 100 g, identical to that measured in normoten sive hypoxemia and significantly less than found during hypotension alone. Cerebral oxygen consumption was lower during combined hypoxemia and cephalic hypoten sion than during hypoxemia alone. Cerebral glucose up take was significantly higher than control in both the hypoxemic and combined hypoxemic-hypotensive condi tions. The glucose:oxygen quotient (6 x molar glucose uptake/molar oxygen consumption) was not different from unity during control or hypotension but was 2.31 ± 1.16 and 3.63 ± 1.99 during the hypoxemic and hypox emic-hypotensive conditions, respectively, suggesting an anaerobic glucose utilization. No significant lactate efflux could be measured in any of these conditions.