Fetal rat brain injury: Effect of transient maternal hypoxemia

Objective: To determine whether transient acute maternal hypoxemia during 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 gestational 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 venous 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 saline and formalin. The brains were embedded in paraffin, sectioned in coronal plane, and stained with hematoxylin and eosin. Histologic assessment of sections was performed by a neuropathologist blinded to the protocol. Statistical analysis of the data was performed using analysis of variance and the chi-square test. Results: Exposure to the gas mixture resulted in decreased maternal pO₂ 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 pCO₂ 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 hippocampus, basal ganglia, thalamus, and hypothalamus in the hypoxemia rats as compared with controls. Conclusion: Transient maternal hypoxemia may cause neuronal necrosis in vulnerable regions of the fetal rat brain, including the hippocampus, basal ganglia, thalamus, and hypothalamus.