Ting P, Yamaguchi S, Bacher J D, Killens R H, Myers R E
Exp Neurol. 1984 Mar;83(3):449-60. doi: 10.1016/0014-4886(84)90114-6.
Our study with midgestational sheep fetuses failed to support a cause-and-effect relation between marked hypoxia with or without hypo- or hypervolemia and rapid surges of blood pressure and the development of germinal matrix or intraventricular hemorrhage. Twenty-nine percent of fetuses exposed to marked hypoxia concomitantly with manipulations of their blood volume and blood pressure developed widespread cerebral necrosis. However, despite this marked anoxic-ischemic brain injury, none developed any germinal matrix or intraventricular hemorrhage. Rapidly and markedly elevating the blood pressure in these fetuses despite the presumed presence of an impaired autoregulation and a probable elevation of their central venous pressure also failed to cause germinal matrix or intraventricular hemorrhage. Marked hypoxia accompanied by reductions in blood pressure brought about by blood withdrawal produced an 80% delayed fetal mortality but not a single instance of germinal matrix or intraventricular hemorrhage.
伴有或不伴有血容量减少或增加的显著缺氧与血压快速波动以及生发基质或脑室内出血的发生之间的因果关系。29%暴露于显著缺氧并同时接受血容量和血压操纵的胎儿发生了广泛的脑坏死。然而，尽管存在这种显著的缺氧缺血性脑损伤，但没有一只胎儿发生任何生发基质或脑室内出血。尽管推测这些胎儿存在自动调节功能受损以及中心静脉压可能升高，但快速且显著地升高其血压也未能导致生发基质或脑室内出血。通过放血导致血压降低的显著缺氧造成了80%的胎儿延迟死亡，但没有一例生发基质或脑室内出血。
