Citation

Okeda R, Matsuo T, Kuroiwa T, Tajima T, Takahashi H. Acta Neuropathol. 1986; 69(3-4): 244-252.

Copyright

(Copyright © 1986, Holtzbrinck Springer Nature Publishing Group)

DOI

unavailable

PMID

3962602

Abstract

The pathogenesis of fetal brain damage caused by acute maternal carbon monoxide (CO) intoxication was experimentally investigated in cats; 11 pregnant cats in various gestational stages were exposed to 0.2-0.3% CO/air gas for 76-150 min; thereafter, 29 live and stillborn neonates and 14 fetuses removed by cesarean section were observed pathologically. In the full-term or late-gestational-stage fetuses and neonates, the most vulnerable areas were the cerebral white matter and brain stem, followed by the basal ganglia and thalamus, and then the cerebral cortex. No changes were found in the cerebellum. From the distribution and nature of the brain changes, a hypoxic-ischemic mechanism was proposed as the pathogenesis of fetal brain damage. In the fetuses or neonates in middle and early gestational stages, the frequency and severity of the brain changes were generally lower than in those in the late gestational stage, and the cerebral white matter and basal ganglia were most often involved, but the thalamus, brain stem and the cerebral cortex were spared. The severity and extent of the brain changes were not the same among all littermates, but varied from normal to severely damaged animals. Among the maternal physiological factors measured during the CO exposure, only the severity of acidosis was correlated with the grade of fetal brain damage.

Language: en