Foetal circulatory responses to arrest of uterine blood flow in sheep: effects of chemical sympathectomy.
Acute foetal asphyxia, caused by arrest of uterine blood flow, increases both sympathetic activity and peripheral vascular resistance and decreases blood flow to peripheral organs (Jensen et al., J. Dev. Physiol., 9, 543-559). The rapidity and uniformity of this peripheral vasoconstriction suggest that the sympatho-neuronal system may reflexly cause these initial blood flow changes during acute asphyxia. To test this hypothesis, we studied 5 intact and 6 chemically sympathectomized (6-hydroxy-dopamine, 46.1 +/- 6 mg/kg foetal weight) chronically prepared normoxaemic foetal sheep in utero at 0.9 of gestation. Organ blood flows (microsphere method), plasma concentrations of catecholamines, vasopressin, and angiotensin II, acid-base balance and blood gases were measured before, during and after arrest of uterine blood flow for 2 min, i.e., at 0, 1, 2, 3, 4 & 30 min. In intact foetuses there was a progressive increase in arterial blood pressure and a rapid circulatory centralization in favour of the brain stem and heart and at the expense of most of the peripheral organs. The changes in peripheral blood flow during and after asphyxia were well reflected by those in the skin and scalp. In chemically sympathectomized foetuses, arterial blood pressure fell transiently at 1 min of asphyxia and cardiac output was redistributed towards the carcass and intestinal organs at the expense of the heart, spinal medulla, and placenta. We conclude that in foetal sheep at 0.9 of gestation, the short-term adaptation to arrest of uterine blood flow is a rapid and profound peripheral vasoconstriction to effect an increase in arterial blood pressure. This initial response during circulatory centralization, which is necessary to increase or maintain blood flow to the heart, brain stem, and placenta, is blunted by sympathectomy. Thus, the foetal sympatho-neuronal system is important for short-term adaptation to and intact survival of asphyxia.
Jensen
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A
Department of Obstetrics and Gynaecology, Justus-Liebig-Universität Giessen, Germany.
Lang
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U
D000222:Adaptation, Physiological; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001237:Asphyxia / Q000503:physiopathology*; D001794:Blood Pressure; D002395:Catecholamines / Q000097:blood; D005260:Female; D005333:Fetus / Q000098:blood supply*; D006706:Homeostasis / Q000502:physiology; D016627:Oxidopamine; D011247:Pregnancy; D012039:Regional Blood Flow; D012756:Sheep / Q000196:embryology; D013563:Sympathectomy, Chemical; D013564:Sympathetic Nervous System / Q000502:physiology*; D014599:Uterus / Q000098:blood supply*; D014661:Vasoconstriction; D014667:Vasopressins / Q000097:blood
D002395:Catecholamines; D014667:Vasopressins; D000804:Angiotensin II; D016627:Oxidopamine