Fetal cardiovascular and metabolic responses to hypoxaemia are central to intact fetal survival and are well conserved across species. For instance, although human labour is commonly associated with transient fetal hypoxaemia caused by uterine contractions, the prevalence of a common manifestation of fetal hypoxaemia, neonatal hypoxic-ischaemic encephalopathy (HIE), is low. It is only when fetal physiological compensations are overwhelmed or blunted that tissue damage occurs, leading to fetal death or long-term disability, such as cerebral palsy. One aspect of the acute cardiovascular defence, the redistribution of cardiac output to favour essential organs such as the adrenals, myocardium and brain, is also central to fetal survival if hypoxaemia is maintained, as observed with fetal growth restriction as a result of placental dysfunction. Any major advance in understanding the mechanisms underlying these responses is therefore to be welcomed.
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