Applied physiology: brain metabolism following perinatal asphyxia

Abstract 

When the fetal or neonatal brain is exposed to a severe transient episode of hypoxia–ischaemia, primary energy failure occurs within minutes leading to depletion of high-energy phosphate compounds. Following resuscitation, mitochondrial function is temporarily restored and energy metabolism returns towards normal. However, a complex series of cytotoxic reactions are initiated within the neuron leading to progressive failure of energy metabolism and ultimately cell death. Elevated cytosolic calcium, free radical release, pro-inflammatory mediators and mitochondrial injury are all implicated in this phase. The progression of encephalopathic signs is closely related to the development of secondary energy failure. If neuroprotective interventions are to be successful, then they must be commenced shortly after resuscitation and they must act at multiple sites within the cytotoxic cascade.

Keywords: neonatal brain, perinatal asphyxia, hypoxiaischaemia, neuroprotection

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• f1 Correspondence to JW. Tel.: +44 (0)20 7679 6113; Fax: +44 (0)20 7679 6103; E-mail: john.wyatt@uclh.org