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绵羊胎儿心率人工诱发晚期减速期间的胎儿氧耗及心率反应机制

Fetal oxygen consumption and mechanisms of heart rate response during artificially produced late decelerations of fetal heart rate in sheep.

作者信息

Parer J T, Krueger T R, Harris J L

出版信息

Am J Obstet Gynecol. 1980 Feb 15;136(4):478-82. doi: 10.1016/0002-9378(80)90674-2.

Abstract

Delayed decelerations of fetal heart rate were produced by abruptly decreasing uterine blood flow to zero for 20 seconds in chronically instrumented, normoxic sheep. Fetal O2 consumption, O2 content, and O2 tension in umbilical blood decreased significantly before the decline in heart rate. Fetal arterial blood pressure did not change significantly. Complete vagal blockade abolished the late deceleration and uncovered a late acceleration, which in turn was eliminated by total beta-adrenergic blockade. We conclude that these late decelerations in normoxic sheep are vagally mediated and due to chemoreceptor rather than baroreceptor activity.

摘要

在长期植入仪器且处于常氧状态的绵羊中,通过突然将子宫血流量降至零持续20秒,可导致胎儿心率出现延迟减速。在心率下降之前,胎儿的氧消耗量、氧含量以及脐血中的氧张力均显著降低。胎儿动脉血压无显著变化。完全迷走神经阻滞可消除晚期减速,并暴露出晚期加速,而晚期加速又可被完全的β-肾上腺素能阻滞消除。我们得出结论,常氧状态下绵羊的这些晚期减速是由迷走神经介导的,且是由于化学感受器而非压力感受器的活动所致。

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