Abstract
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).
Highlights
Suboptimal in utero growth is well understood to have long-lasting physiological implications for the developing fetus and the subsequent newborn and adult
This review examines the mechanisms underpinning the cardiovascular and cerebrovascular dysfunction associated with fetal growth restriction and brain sparing (Figure 1)
This review highlights the impact of these physiological adaptations to the developing fetal cardiovascular and cerebrovascular systems, as well as emerging long-term effects in offspring that were growth restricted at birth
Summary
Suboptimal in utero growth is well understood to have long-lasting physiological implications for the developing fetus and the subsequent newborn and adult. This narrative review will focus on the impacts of fetal growth restriction (FGR) on the cardiovascular and cerebrovascular system. Optimal placental function and uteroplacental blood flow are essential for the maintenance of an adequate supply of oxygen and nutrients to support fetal development and growth. Any impairment in this supply can result in fetal hypoglycaemia and hypoxaemia [12]. The benefits and limitations of pre-clinical animal models of FGR have previously been reviewed [13]
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