A normal birth produces a change from the relatively hypoxic intrauterine state of the fetus, to the better-oxygenated condition of the healthy newborn baby. Cerebral artery blood flow velocity is substantially reduced after birth but increases thereafter in healthy term infants. Oxygen delivery to the brain is prioritized as it is sensitive to hypoxic damage particularly around the time of birth. Reductions in cerebral oxygen delivery occur when hypoxia is severe, particularly when it is combined with brain ischemia. If the redistributory response is inadequate or if reductions in cardiac output are severe or repeated, then a combination of reduced brain blood flow and hypoxia may lead to brain injury. This review also examines the relationship between hypoxicischemic encephalopathy (HIE) and the disruption of the bloodbrain barrier (BBB). The extent of injury noted in HIE is not only determined by the biochemical cascades that trigger the apoptosis-necrosis continuum of cell death in the brain parenchyma but also by the breaching of the BBB by proinflammatory factors. The role of factors such as HIF-1α and VEGF are also explored.
|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||6|
|State||Published - Jan 1 2021|
ASJC Scopus subject areas