FETAL-RAT BRAIN INJURY - EFFECT OF TRANSIENT MATERNAL HYPOXEMIA

Objective: To determine whether transient acute maternal hypoxemia dur ing the end of pregnancy may cause neuronal damage in fetal rat brains . Study Design: Nine pregnant rats (4 study and 5 controls) at 16-17 g estational days were studied. The study rats were placed in a chamber and breathed a gas mixture of 11.8% oxygen, 4.95% CO2,and nitrogen for either 1 or 2 h, while the control animals breathed room air. Tail ve nous blood was collected and gases were evaluated at the beginning and conclusion of the exposure periods. After 72 h of recovery, at 19-20 days' gestation, the fetal cardiovascular systems were perfused with s aline and formalin. The brains were embedded in paraffin, sectioned in coronal plane, and stained with hematoxylin and eosin. Histologic ass essment of sections was performed by a neuropathologist blinded to the protocol. Statistical analysis of the data was performed using analys is of variance and the chi-square test. Results: Exposure to the gas m ixture resulted in decreased maternal pO(2) from 39.9 +/- 7.6 mm Hg in the control group to 28.8 +/- 2.0 mm Hg in the 2-hour hypoxia group ( p < 0.05). No significant changes in maternal pH or pCO(2) status have been noted. A total of 34 fetal rat brains served as controls and 26 brains as the hypoxia study group. There was a significant increase in isolated neuronal damage, including necrosis and shrinkage of cells, with karyorrhexis (fragmentation and breakage of the nucleus) in the h ippocampus, basal ganglia, thalamus, and hypothalamus in the hypoxemia rats as compared with controls. Conclusion: Transient maternal hypoxe mia may cause neuronal necrosis in vulnerable regions of the fetal rat brain, including the hippocampus, basal ganglia, thalamus, and hypoth alamus.