![]() ![]() One of the most common challenges to the fetus during late gestation is an episode of O 2 deprivation. In conclusion, the data support our hypothesis and show that acute acidemia markedly alters fetal hemodynamic, metabolic, and endocrine responses to acute hypoxemia. Acidemia also reversed the increase in umbilical vascular conductance during hypoxemia to vasoconstriction. 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. Treatment with acidified saline reduced fetal basal pH from 7.35 ± 0.01 to 7.29 ± 0.01 but did not alter basal cardiovascular variables, blood glucose, or plasma concentrations of catecholamines, ACTH, and cortisol. After 5 days, animals were subjected to an acute hypoxemia protocol during intravenous infusion of saline or treatment with acidified saline. Under general anesthesia, five sheep fetuses at 0.8 gestation were instrumented with catheters and Transonic flow probes around the femoral and umbilical arteries. 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. This study tested the hypothesis that fetal acidemia affects the fetal defense responses to acute hypoxemia. However, the effects on the fetal defense responses to acute hypoxemia during fetal acidemia are not well understood. There is growing clinical concern about the combined effects of fetal hypoxemia and fetal acidemia on neonatal outcome. In complicated pregnancy, fetal hypoxemia rarely occurs in isolation but is often accompanied by fetal acidemia. ![]()
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