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The early time period following ischemia may be of pathogenetic importance in hypoxic-ischemic brain injury. Global cerebral oligemia was induced in ten late gestation fetal sheep by inflation of a balloon occluder around the brachiocephalic artery. Cerebral blood flow, oxygen, glucose, and lactate net flux, and oxygen delivery were measured by the Fick principle following 1 h of oligemia and at 5, 30, and 60 min of postoligemic reperfusion. During oligemia, cerebral blood flow decreased by 74 ± 10% (mean ± SD) and oxygen consumption decreased by 34 ± 24%. The glucose:oxygen quotient was elevated throughout the oligemic period. In the early (5 min) reperfusion period, blood flow and oxygen delivery were not different from control but oxygen consumption was persistently depressed by 27 ± 32%; fractional extraction of oxygen was 0.38 ± 0.10 during control and 0.24 ± 0.09 during early reperfusion. The venous oxygen tension increased modestly from 15.2 ± 2.4 to 18.0 ± 1.7 mm Hg; the postoligemic venous pO 2  was limited by the lack of reactive hyperemia combined with the low arterial pO 2  of the intrauterine environment. Postoligemic carbohydrate fluxes could not be differentiated from control, possibly due to blood–brain barrier limitations. These factors may be related to the relative resistance of the fetal brain to hypoxic–ischemic injury.

Fetal Cerebral Blood Flow and Metabolism during Oligemia and Early Postoligemic Reperfusion