EFFECT OF MATERNAL HYPOXIA ON FETAL RAT BRAINS

Abstract

Cerebral metabolic and neuropathologic changes in fetal rats were examined during and following maternal hypoxia. Term pregnant rats were tracheostomized or intubated, paralyzed, and artificially ventilated with 40%, 15% or 10% O₂-balance N₂O. Maternal acid-base and cardiovascular status was monitored. Dams then were subjected to C-section or allowed to recover and deliver spontaneously.

Dams exposed to 15% O₂ for 60 minutes were hypoxic (paO₂=38mmHg) and acidotic (pHa=7.22mmHg). MABP fell by 25%. In fetal brain, lactate (L) and pyruvate (p) increased, but disproportionately such that the L/P ratio increased 10 fold. Brain glucose and glycogen decreased. Both ATP and P-Creatine decreased, indicating a disruption of the energy state of the brain.

In resuscitated dams, fetal survival at delivery was 86%. Sequential measurements of postnatal growth and development of surviving pups were the same as offspring of control dams. No histologic alterations of hypoxia-ischemia were found in brains of pups sacrificed at 30 days; hypomyelinization of ascending ana descending spinal cord pathways was seen in a few animals. In dams exposed to 10% O₂ for 30 minutes, systemic hypoxia was more severe (paO₂=30mmHg), but pHa and MABP were comparable to levels obtained in dams exposed to 15% O₂ for 60 minutes. Changes in glycolytic intermediates and high energy metabolites of fetal brains as well as functional parameters were comparable to fetuses of dams exposed to 15% O₂ for 60 minutes.

The findings indicate that although maternal hypoxia leads to major alterations in the energy status of the fetal brain, this does not necessarily culminate in overt brain damage.

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