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The Role of Nitric Oxide on Fetal Cardiovascular Control During Normoxia and Acute Hypoxia in 0.75 Gestation Sheep

Y. Garnier, MD

S. Supçun, MD

A. Jensen, MD

Department of Obstetrics and Gynecology, University of Maastricht, Maastricht, The Netherlands, and Department of Obstetrics and Gynecology, University of Bochum, Bochum, Germany

T. H. M. Hasaart, MD, PhD

Department of Obstetrics and Gynecology, University of Maastricht, Maastricht, The Netherlands, and Department of Obstetrics and Gynecology, University of Bochum, Bochum, Germany; University Hospital Maastricht, PO Box 5800, P. Debyelaan 25, 6202 AZ Maastricht, The Netherlands; thas{at}sgyn.azm.nl

R. Berger, MD

Department of Obstetrics and Gynecology, University of Maastricht, Maastricht, The Netherlands, and Department of Obstetrics and Gynecology, University of Bochum, Bochum, Germany

Objective: The role of nitric oxide in control of fetal cardiovascular functions and of cerebral blood flow during normoxia and acute hypoxia is only partially known. We studied the effects of nitric oxide synthase inhibition on the distribution of cardiac output in preterm sheep using N-nitro-L-arginine methyl ester (L-NAME).

Methods: Thirteen fetal sheep were instrumented at a gestational age of 107 days. Three days later fetuses received L-NAME (n = 7) or vehicle infusion (n = 6). At 0 minutes, acute hypoxia was induced by occasion of the maternal aorta for 2 minutes. Organ blood flows (microsphere method) and physiologic variables (fetal heart rate, mean arterial pressure [MAP], oxygen saturation, and pH) were measured at -75, -1, +2, +4, and +30 minutes.

Results: L-NAME caused bradycardia and an increase in MAP. A significant decrease in cardiac output by 32% occurred in the control group during the control period, which was consequently reflected in organ blood flows. L-NAME injection reduced cardiac output by 64% during normoxia. Blood flow to the fetal body, placenta, and cerebrum decreased by 62%, 66%, and 55%, respectively. During acute hypoxia, L-NAME did not change the redistribution of cardiac output toward the central organs. In the L-NAME group MAP increased, and fetal heart rate was maintained; in contrast, in controls MAP initially decreased and then returned to control values while fetal heart rate decreased. After hypoxia L-NAKE delayed the recovery of cardiac output and blunted the increase in blood flow to the brain and heart.

Conclusion: Although influenced by fetal stress after extensive instrumentation, the results of this study indicate that nitric oxide plays a role in fetal cardiovascular control during normoxia and acute hypoxia. Nitric oxide also mediates the increase in blood flow to the brain and heart immediately after hypoxia.

Key Words: Fetus • nitric oxide • hypoxia • organ blood flow

Journal of the Society for Gynecologic Investigation, Vol. 10, No. 5, 275-282 (2003)
DOI: 10.1016/S1071-55760300085-6


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