Is the Rapid and Intense Peripheral Vasoconstriction Occurring during Acute Hypoxaemia in the Llama Fetus an Arterial Chemoreflex?

Giussani, Dino A.; Riquelme, Raquel; Hanson, Mark A.; Llanos, Aníbal J.

doi:10.1007/978-1-4615-2572-1_62

Cited by 3 publications

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“…In late gestation, the fetal cardiovascular defense to acute hypoxemia is triggered via a carotid chemoreflex, resulting in transient bradycardia and redistribution of the cardiac output toward essential circulations, such as those perfusing the fetal brain, heart, and adrenal glands, at the expense of peripheral vascular beds. Once initiated, the peripheral vasoconstriction is maintained by the release of vasoactive agents into the fetal circulation (6,7,23,24). In addition, umbilical blood flow is maintained during acute hypoxemia or elevated when the severity of the hypoxemic challenge increases as a result of the combined effects of increased perfusion pressure and activity of nitric oxide across the umbilical vascular bed (48).…”

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Effects of acute acidemia on the fetal cardiovascular defense to acute hypoxemia

Thakor¹,

Giussani²

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Thakor AS, Giussani DA. Effects of acute acidemia on the fetal cardiovascular defense to acute hypoxemia. Am J Physiol Regul Integr Comp Physiol 295: R90 -R99, 2009. First published October 15, 2008 doi:10.1152/ajpregu.90689.2008.-In complicated pregnancy, fetal hypoxemia rarely occurs in isolation but is often accompanied by fetal acidemia. There is growing clinical concern about the combined effects of fetal hypoxemia and fetal acidemia on neonatal outcome. However, the effects on the fetal defense responses to acute hypoxemia during fetal acidemia are not well understood. This study tested the hypothesis that fetal acidemia affects the fetal defense responses to acute hypoxemia. The hypothesis was tested by investigating, in the late-gestation sheep fetus surgically prepared for long-term recording, the in vivo effects of acute fetal acidemia on 1) the fetal cardiovascular responses to acute hypoxemia and 2) the neural and endocrine mechanisms mediating these responses. Under general anesthesia, five sheep fetuses at 0.8 gestation were instrumented with catheters and Transonic flow probes around the femoral and umbilical arteries. After 5 days, animals were subjected to an acute hypoxemia protocol during intravenous infusion of saline or treatment with acidified saline. Treatment with acidified saline reduced fetal basal pH from 7.35 Ϯ 0.01 to 7.29 Ϯ 0.01 but did not alter basal cardiovascular variables, blood glucose, or plasma concentrations of catecholamines, ACTH, and cortisol. During hypoxemia, treatment with acidified saline increased the magnitude of the fetal bradycardia and femoral vasoconstriction and concomitantly increased chemoreflex function and enhanced the increments in plasma concentrations of catecholamines, ACTH, and cortisol. Acidemia also reversed the increase in umbilical vascular conductance during hypoxemia to vasoconstriction. In conclusion, the data support our hypothesis and show that acute acidemia markedly alters fetal hemodynamic, metabolic, and endocrine responses to acute hypoxemia.

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