Fetal brain injury after maternal carbon monoxide intoxication. Clinical and neuropathologic aspects.
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.
D000818:Animals; D001479:Basal Ganglia / Q000473:pathology; D001925:Brain Damage, Chronic / Q000139:chemically induced* / Q000473:pathology; D002249:Carbon Monoxide Poisoning / Q000473:pathology; D002263:Carboxyhemoglobin / Q000032:analysis; D002421:Caudate Nucleus / Q000473:pathology; D002540:Cerebral Cortex / Q000473:pathology; D005260:Female; D005312:Fetal Blood / Q000032:analysis; D005315:Fetal Diseases / Q000139:chemically induced* / Q000473:pathology; D005311:Fetal Hypoxia / Q000139:chemically induced; D005917:Globus Pallidus / Q000473:pathology; D000882:Haplorhini; D008253:Macaca mulatta; D008431:Maternal-Fetal Exchange; D010108:Oxyhemoglobins / Q000032:analysis; D011247:Pregnancy; D011248:Pregnancy Complications; D011699:Putamen / Q000473:pathology; D013788:Thalamus / Q000473:pathology
D010108:Oxyhemoglobins; D002263:Carboxyhemoglobin