Ginsberg M D, Myers R E
Neurology. 1976 Jan;26(1):15-23. doi: 10.1212/wnl.26.1.15.
In a model of brain damage in the rhesus monkey fetus, carbon monoxide inhalation by the mother was used to produce graded fetal hypoxia. Four fetuses with aterial oxygen contents of 2.1 to 2.4 ml per 100 ml during the most severe insult hour appeared neurologically normal, and their brains contained no lesions. A single animal with an intermediate degree of hypoxia was moderately abnormal; its brain showed extensive necrosis of the basal ganglia. Four fetuses with arterial oxygen contents of 1.6 to 1.8 ml per 100 ml during the most severe insult hour showed profound clinical deficits, and on postmortem examination the brains were markedly swollen and showed an extensive hemorrhagic necrosis. The fetal brain exhibits a high threshold to the effects of sustained hypoxia, but once a critical level of deoxygenation is exceeded, extensive brain damage with early death results.
在恒河猴胎儿脑损伤模型中，通过让母体吸入一氧化碳来造成不同程度的胎儿缺氧。在最严重缺氧的一小时内，动脉血氧含量为每100毫升2.1至2.4毫升的四只胎儿神经功能正常，其大脑无损伤。一只缺氧程度中等的动物表现为中度异常；其大脑基底神经节出现广泛坏死。在最严重缺氧的一小时内，动脉血氧含量为每100毫升1.6至1.8毫升的四只胎儿出现严重的临床缺陷，尸检显示大脑明显肿胀并出现广泛的出血性坏死。胎儿脑对持续缺氧的影响具有较高的阈值，但一旦超过临界脱氧水平，就会导致广泛的脑损伤并早期死亡。
