Abstract
This study assesses the vulnerability of fetal guinea pig heart to metabolic changes during acute nonlethal in utero hypoxia. Guinea pigs (50–55 days gestation) were exposed to 7% O<sub>2</sub> for 2 h and room air for 4 h. Fetal hearts were harvested before hypoxia, at the end of hypoxia, and 4 h after hypoxia, and analyzed for: apoptosis (TUNEL), histology, lipid peroxidation and ATP. A group of posthypoxic dams was taken to gestation. Within 48 h postpartum, the function of neonatal hearts was tested and cerebral histology examined. Fetal heart ATP was decreased by 27% at the end of hypoxia and by 32% 4 h after hypoxia. The lipid peroxides, 4-hydroxynonenal and malondialdehyde, were decreased by 37 and 46%, respectively, by 4 h after hypoxia. The apoptotic index increased from 2% in prehypoxic hearts to 8.4% by 4 h after hypoxia. Fetal heart morphology was unremarkable. Postpartum neonatal cardiac function was not affected and cerebral histology was unremarkable. These results support the conclusion that nonlethal in utero hypoxia has acute effects on the fetal heart but no persistent cardiac or cerebral effects in the postpartum neonate.
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