The Role of Nitric Oxide on Fetal Cardiovascular Control During Normoxia and Acute Hypoxia in 0.75 Gestation Sheep
| Autor: | S. Supçun, A. Coumans, Richard Berger, T. H. M. Hasaart, Arne Jensen, Yves Garnier |
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| Rok vydání: | 2003 |
| Předmět: |
medicine.medical_specialty
Cardiac output Mean arterial pressure Placenta Blood Pressure Gestational Age Biology Fetal Hypoxia Nitric Oxide Cardiovascular System Nitric oxide chemistry.chemical_compound Fetal Heart Pregnancy Internal medicine Heart rate medicine Animals Cardiac Output Enzyme Inhibitors Sheep Obstetrics and Gynecology Blood flow Carbon Dioxide Heart Rate Fetal Hydrogen-Ion Concentration Hypoxia (medical) Fetal Blood Oxygen NG-Nitroarginine Methyl Ester Endocrinology chemistry Cerebral blood flow Regional Blood Flow Circulatory system Female Nitric Oxide Synthase medicine.symptom |
| Zdroj: | Journal of the Society for Gynecologic Investigation. 10:275-282 |
| ISSN: | 1071-5576 |
| Popis: | 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(omega)-nitro-L-arginine methyl ester (L-NAME).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 occlusion 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.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-NAME delayed the recovery of cardiac output and blunted the increase in blood flow to the brain and heart.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. |
| Databáze: | OpenAIRE |
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