title: The premature fetus: not as defenseless as we thought, but still paradoxically vulnerable?
abstract: Traditionally, it has been believed that the cardiovascular and hormonal responses to asphyxia in preterm fetuses are immature, and this immaturity contributes to their apparent vulnerability to neural injury. However, these data were derived from studies using relatively mild insults, which did not allow for the greater cardiac glycogen reserves and anaerobic capacity of the brain near midgestation. Here, we review the maturation of the cardiovascular and cerebrovascular and cerebral responses to asphyxia in experimental animals and how these relate to the apparent vulnerability of the human premature brain. Most such investigations have been performed in the chronically instrumental fetal sheep. Recent studies have demonstrated that the premature fetus has highly adaptive and relatively mature responses to asphyxia, and that in absolute terms the preterm brain is very resistant to asphyxial injury. These data suggest that the premature fetus is able to survive much more prolonged periods of asphyxia than the near-term fetus, but that, paradoxically, such survival is associated with exposure to prolonged periods of hypotension and hypoperfusion and consequently greater risk of severe neural damage.
authors.affiliation: Liggins Institute and Department of Pediatrics, University of Auckland, New Zealand. aj.gunn@auckland.ac.nz
authors.forename: A J
authors.initials: AJ
authors.lastname: Gunn
authors.forename: J S
authors.initials: JS
authors.lastname: Quaedackers
authors.forename: J
authors.initials: J
authors.lastname: Guan
authors.forename: E
authors.initials: E
authors.lastname: Heineman
authors.forename: L
authors.initials: L
authors.lastname: Bennet
mesh_terms: D000818:Animals; D001238:Asphyxia Neonatorum / Q000503:physiopathology*; D001921:Brain / Q000254:growth & development*; D002319:Cardiovascular System / Q000254:growth & development*; D006801:Humans; D007231:Infant, Newborn; D007234:Infant, Premature / Q000502:physiology*