The neonatal gastrointestinal (GI) system can be vulnerable to injury from hypoxic respiratory failure and birth asphyxia (1). Changes in intestinal hemodynamics occur during the transition from fetal to postnatal life as the newborn infant switches the source of nutrition from the placenta to the GI tract (2, 3). Intestinal vascular resistance is high in fetal life and rapidly decreases after birth. This postnatal decrease occurs in part because of increased endothelial production of nitric oxide, a vasodilator (3, 4). This low intestinal vascular resistance affects the ability of the neonatal intestinal vasculature to respond to systemic circulatory changes, such as hypotension, arterial hypoxemia, and hypoxia. Newborn infants have immature pressure-flow autoregulation in response to hypotension, resulting in decreased oxygen delivery to the intestines (5). In neonatal swine studies, severe hypoxemia causes newborns to respond with vasoconstriction, leading to intestinal ischemia (1). Hypoxia and ischemia occurring in the fetus and newborn can further reduce intestinal perfusion by eliciting a “diving reflex” that preferentially diverts blood flow away from organs such as the intestines to preserve blood flow to the brain, heart, and adrenals (6). It is unclear whether the diving reflex causes necrosis of the intestine, but developmental alterations in the microcirculation have been hypothesized to dispose to intestinal necrosis (3).
|Original language||English (US)|
|Title of host publication||Hypoxic Respiratory Failure in the Newborn|
|Subtitle of host publication||From Origins to Clinical Management|
|Number of pages||3|
|State||Published - Jan 1 2021|
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