Foetal hypoxia is an important determinant of birth asphyxia and subsequent adverse outcome: antenatal neuroprotection at term

Hypoxic-ischaemic encephalopathy is directly associated with the development of cerebral palsy and cognitive disabilities later in life, therefore remaining an important problem in perinatal medicine. Postnatal neuroprotective strategies have been investigated elaborately, but up to now, only moderate hypothermia proved to be beneficial in reducing post hypoxic-ischaemic encephalopathy in a selected group of asphyxiated neonates. Since the vast amount of toxic free radicals is produced in the reperfusion and reoxygenation period upon and immediately (30–60 min) after birth, we postulate that antenatal (i.e. maternal) pharmacologic neuroprotection of the foetus, combined with postnatal hypothermia, might be a more optimal approach to prevent this free radical induced brain damage. This review summarizes the molecular mechanisms underlying early reperfusion–reoxygenation damage and focuses on the most promising pharmacologic agents (phenobarbital, vitamin C and E, allopurinol, melatonin and xenon) to be given antenatally to the mother to neuroprotect the hypoxic foetus.