Key result
Fetal brain sparing preserves cerebral blood flow but triggers long-term cardiovascular and neurological impairment.
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Fetal growth restriction (FGR) is a common complication of pregnancy, resulting in a fetus that fails to reach its genetically determined growth potential. Whilst the fetal cardiovascular response to acute hypoxia is well established, the fetal defence to chronic hypoxia is not well understood due to experiment constraints. Growth restriction results primarily from reduced oxygen and nutrient supply to the developing fetus, resulting in chronic hypoxia. The fetus adapts to chronic hypoxia by redistributing cardiac output via brain sparing in an attempt to preserve function in the developing brain. This review highlights the impact of brain sparing on the developing fetal cardiovascular and cerebrovascular systems, as well as emerging long-term effects in offspring that were growth restricted at birth. Here, we explore the pathogenesis associated with brain sparing within the cerebrovascular system. An increased understanding of the mechanistic pathways will be critical to preventing neuropathological outcomes, including motor dysfunction such as cerebral palsy, or behaviour dysfunctions including autism and attention-deficit/hyperactivity disorder (ADHD).
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Rock et al. (2021) conducted a review in Fetal growth restriction. Brain sparing in fetal growth restriction was evaluated on Cardiovascular, cerebrovascular, and neuropathological outcomes. Brain sparing in fetal growth restriction redistributes cardiac output to preserve the developing brain, but induces long-term cardiovascular, cerebrovascular, and neuropathological effects.
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