Effects of beta-adrenergic blockade on blood flow distribution during hypoxaemia in fetal sheep.
Effects of beta-adrenergic blockade on blood flow distribution during hypoxaemia in fetal sheep.
复制标题
β-肾上腺素能阻断对胎羊低氧血症期间血流分布的影响。
DOI：
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
A. Llanos
中科院分区：
文献类型：
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作者：
D. J. Court;J. Parer;B. S. Block;A. Llanos
胎羊的低氧血症会导致心脏、大脑和肾上腺的血管阻力降低，从而导致流向这些器官的血流增加。胎盘血流得以维持。为了研究低氧血症期间β-肾上腺素能活性增加是否参与这些变化，在妊娠126至130天的5只长期插管胎羊中研究了普萘洛尔对胎儿低氧血症（胎儿血红蛋白饱和度降低50%）期间器官血流量（使用微球方法）和其他心血管变量的影响。低氧血症期间β受体阻滞剂导致胎儿心动过缓和心输出量下降30%。胎盘和心肌血流量分别下降了39%和37%。总外周阻力增加35%，主要是由于胎儿胎盘血管阻力增加。心得安可增加心、肺血管阻力。在3只类似的插管动物中，在没有低氧血症的情况下给予普萘洛尔导致心输出量和胎盘血流量下降9%，但没有血流重新分布到胎儿器官。它的结论是，增加β-肾上腺素能活性与胎儿低氧血症限制伴随增加迷走神经活动的负变时作用，保持胎盘血流通过其变力性和变时性活动，以及通过维护胎盘血管舒张，并可能是几个因素之一，增加心肌血流量在低氧血症。
Hypoxaemia in fetal sheep causes a decrease in vascular resistance of the heart, brain and adrenal gland which results in increased blood flow to these organs. Placental blood flow is maintained. To investigate whether increased beta-adrenergic activity during hypoxaemia is involved in these changes, the effects of propranolol on organ blood flows (using the microsphere method) and other cardiovascular variables were studied during fetal hypoxaemia (50% reduction of fetal haemoglobin saturation) in 5 chronically catheterized fetal sheep at 126 to 130 days of gestation. Beta-blockade during hypoxaemia caused a fetal bradycardia and a 30% drop in cardiac output. Placental and myocardial blood flows fell by 39% and 37% respectively. Total peripheral resistance increased by 35% mainly due to increased fetal placental vascular resistance. Heart and lung vascular resistances increased following propranolol. In 3 similarly catheterized animals, propranolol administered in the absence of hypoxaemia led to a 9% drop in cardiac output and placental blood flow but no redistribution of blood flow to fetal organs. It is concluded that the increased beta-adrenergic activity associated with fetal hypoxaemia limits the negative chronotropic effects of concomitantly increased vagal activity, maintains placental blood flow through its inotropic and chronotropic activity as well as by maintenance of placental vasodilatation and may be one of several factors which increase myocardial blood flow during hypoxaemia.