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Am J Physiol Regul Integr Comp Physiol 281: R381-R390, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 2, R381-R390, August 2001

Fetal cerebral and peripheral circulatory responses to hypoxia after nitric oxide synthase inhibition

Andrew P. Harris1, Sabah Helou2, Christine A. Gleason3, Richard J. Traystman1, and Raymond C. Koehler1

Departments of 1 Anesthesiology and Critical Care Medicine and 2 Pediatrics, The Johns Hopkins University, Baltimore, Maryland 21287; and the 3 Department of Pediatrics, University of Washington, Seattle, Washington 98195

The increase in cerebral blood flow (CBF) during hypoxia in fetal sheep at 0.6 gestation is less than the increase at 0.9 gestation when normalized for differences in baseline CBF and oxygen consumption. Nitric oxide (NO) synthase (NOS) catalytic activity increases threefold during this period of development. We tested the hypothesis that administration of the NOS inhibitor Nomega -nitro-L-arginine methyl ester (L-NAME) decreases the CBF response to systemic hypoxia selectively at 0.9 gestation. We also tested whether any peripheral vasoconstriction during hypoxia is potentiated by L-NAME at 0.9 gestation. Administration of L-NAME increased arterial blood pressure and decreased microsphere-determined CBF during normoxia in fetal sheep at both 0.6 and 0.9 gestation. With subsequent reduction of arterial oxygen content by ~50%, the percent increase in forebrain CBF in a control group (57 ± 11%; ± SE) and L-NAME-treated group (51 ± 6%) was similar at 0.6 gestation. Likewise, at 0.9 gestation, the increase in CBF was similar in control (90 ± 25%) and L-NAME (80 ± 28%) groups. At 0.9 gestation, L-NAME treatment attenuated the increase in coronary blood flow and increased gastrointestinal vascular resistance during hypoxia. We conclude that NO exerts a basal vasodilatory influence in brain as early as 0.6 gestation in fetal sheep but is not an important mechanism for hypoxic vasodilation in brain at either 0.6 or 0.9 gestation. Thus the developmental increase in NOS catalytic capacity does not appear to be responsible for developmental increases in the CBF response to hypoxia during this period. In contrast, NO modulates the vascular response to hypoxia in heart and gastrointestinal tract.

cerebral blood flow; coronary blood flow; fetus; gastrointestinal blood flow; sheep


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