Block B S, Schlafer D H, Wentworth R A, Kreitzer L A, Nathanielsz P W
Department of Gynecology and Obstetrics, Loma Linda University, Ca 92359.
J Dev Physiol. 1990 Feb;13(2):81-5.
To determine the capacity of the fetus to adapt to chronic O2 deficiency produced by decreased placental perfusion in the early development of growth retardation, we embolized the umbilical placental vascular bed of fetal sheep for a period of 9 days. Fetal umbilical placental embolization decreased arterial O2 content by 39%, decreased total placental blood flow by 33%, and produced a 20% reduction in mean fetal body weight. Neither the combined ventricular output nor the regional blood flow distribution was significantly different between the 8 growth-retarded and 7 normally grown fetuses despite the 39% decrease in fetal arterial O2 content. Thus a 33% reduction in total placental blood flow restricts normal fetal growth, but does not exceed the placental circulatory reserve capacity necessary to maintain normal basal metabolic oxygenation. Because the proportion of combined ventricular output to the placenta at rest is decreased in late IUGR fetuses but not in early IUGR fetuses, despite chronic oxygen deficiency, we conclude that the growth retarded fetus maintains a normal regional blood flow distribution until the placental circulatory reserve capacity is depleted.
为了确定胎儿在生长迟缓早期因胎盘灌注减少而适应慢性缺氧的能力,我们对胎羊的脐胎盘血管床进行了为期9天的栓塞。胎儿脐胎盘栓塞使动脉血氧含量降低了39%,胎盘总血流量降低了33%,胎儿平均体重降低了20%。尽管胎儿动脉血氧含量降低了39%,但8只生长迟缓胎儿和7只正常生长胎儿的心室联合输出量和局部血流分布均无显著差异。因此,胎盘总血流量降低33%会限制胎儿正常生长,但未超过维持正常基础代谢氧合所需的胎盘循环储备能力。由于晚期宫内生长受限胎儿静息时心室联合输出量与胎盘的比例降低,而早期宫内生长受限胎儿则未降低,尽管存在慢性缺氧,我们得出结论,生长迟缓胎儿在胎盘循环储备能力耗尽之前维持正常的局部血流分布。