Acute hypoxemia results in hypertension, bradycardia, and cardiac output redistribution in fetal sheep. The blood flow redistribution is produced by differential changes in vascular resistance of various fetal organs. alpha-Adrenergic activity is one of the few vasoconstrictor mechanisms thus far identified in the hypoxemic fetal sheep. Arginine vasopressin (AVP) is a potent vasoconstrictor in adults. Since AVP administration to the normoxic fetus mimics some of the fetal cardiovascular responses to hypoxemia and fetal plasma AVP levels increase with hypoxemia, we examined the hypothesis that AVP modifies the fetal cardiovascular response to hypoxemia by changing the vascular resistance of some fetal vascular beds. To test this we determined fetal systemic arterial pressure and fetal cardiac output and its distribution during hypoxemia with and without the V1 AVP antagonist d(CH2)5-Tyr(Me)AVP. Fourteen fetal sheep (0.79-0.90 of gestation) were chronically catheterized. Five days after surgery fetal hypoxemia was induced by introducing a mixture of 95% N2-5% CO2 (10-20 l/min) into a maternal tracheal catheter. The hypoxemia was maintained for 40 min. Fetal heart rate, systemic arterial blood pressure, and combined ventricular output and its distribution (radiolabeled microspheres) were measured before hypoxemia, at 20 min of hypoxemia alone, and at 20 min of hypoxemia plus either AVP antagonist (n = 5) or NaCl 0.9% (n = 5, controls). Fetal hypertension and bradycardia were partially reversed after the AVP antagonist administration during hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)
The fetal llama exposed to an intense degree of hypoxaemia did not increase cerebral blood flow, but showed a marked peripheral vasoconstriction. The same cardiovascular response is observed in fetal sheep submitted to a extremely severe hypoxaemia, when the initial compensatory vasodilatory mechanisms in brain and heart fail. To investigate whether the fetal llama responses to acute hypoxaemia are adaptive, or whether they are the result of a breakdown of mechanisms of blood flow redistribution that favours the central nervous system, we studied seven fetal llamas (0.6-0.7 of gestation) chronically-catheterized during 1 h of graded and progressive hypoxaemia. Fetal ascending aorta blood gases and fetal cardiac output and its distribution (radiolabelled-microspheres) were measured after 60 min of normoxaemia (B) and at the end of 20 min (H20), 40 min (H40) and 60 min (H60) of hypoxaemia. Data were analysed by ANOVA and Newman-Keuls tests. Each treatment resulted in a lower (P < 0.05) percentage of haemoglobin saturation than hypoxaemia; H40 was lower than H20, and H60 was lower than H20 and H40. No statistical difference was observed among treatments for cardiac output or cerebral blood flow. These results demonstrate that fetal cardiac output and brain blood flow are maintained at all degrees of hypoxaemia, indicating that these cardiovascular responses are an adaptive response in the llama fetus, rather than an index of cardiorespiratory decompensation.
Intravenous administration of the opioid receptor antagonist naloxone to asphyxiated fetal sheep increases the arterial blood pressure. We examined the hypothesis that endogenous opioids modify the cardiac output distribution during asphyxia due to changes in the vascular resistance of some fetal organs. Thirteen fetal sheep (0.8-0.9 of gestation) were chronically catheterized. Fetal asphyxia was induced by reducing the uterine blood flow with an inflatable occluder around the common internal iliac artery to approximately 50% of control for 40 min. Naloxone solution or the solvent alone was added for the last 20 min. Asphyxia caused hypertension, and the fetal arterial blood pressure further increased when asphyxiated fetuses received naloxone. Heart, brain, and adrenal blood flows increased due to the increase in blood pressure, with no changes in their vascular resistances. In contrast, kidney and carcass blood flows decreased, and their vascular resistances increased. We conclude that endogenous opioids inhibit the vasoconstriction of these vascular beds during fetal asphyxia.
INl'RAViWl'RICOIAR HPDRRHPI;E A5 A CAUSE OF tIYDmI.Pf1AUIS IN 17 P~~R N S . B u s t o s , R . Uruguayan Center of Perhatology (CUP), mntevideo,Uruguay.Ultrasonography has been widely used to d e t e c t i n t r a c r a n i a l disease, s p s c i a l l y i n t r a c r a n i a l herorrhage, in p r m t u r e m t c s and h a been
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