title: Cerebral autoregulation in the first day after preterm birth: no evidence of association with systemic inflammation.
abstract: BACKGROUND
  Both systemic inflammation and impaired cerebral autoregulation (CA) have been associated with brain injury in preterm infants. We hypothesized that impaired CA represents a hemodynamic link between inflammation and brain injury.
  
  
  RESULTS
  Neither fetal vasculitis nor interleukin-6 (IL-6) affected CA significantly. A high level of IL-6 was associated with hypotension (P = 0.03) irrespective of dopamine therapy. The magnitude of impairment in CA increased with decreasing mean arterial blood pressure (MAP) (P = 0.02). No significant associations were found between these parameters and either intraventricular hemorrhage (IVH) (n = 10) or neonatal mortality (n = 8).
  
  
  CONCLUSIONS
  In conclusion, postnatal inflammation was weakly associated with arterial hypotension, and hypotension was weakly associated with impaired autoregulation. There was no direct association, however, between autoregulation and antenatal or postnatal signs of inflammation.
  
  
  METHODS
  In our study, 60 infants (mean (±SD) of gestational age (GA) 27 (±1.3) wk) underwent continuous recording of MAP and cerebral oxygenation index (OI) by means of near-infrared spectroscopy (NIRS) for 2.3 ± 0.5 h, starting 18 ± 9 h after birth. Coherence and transfer function gain between MAP and OI represented the presence and degree of impairment of CA, respectively. We considered fetal vasculitis (placenta histology) to be an antenatal marker of inflammation, and used the level of IL-6 in blood, measured at 18 ± 10 h after birth, as a postnatal marker of inflammation. Definition of hypotension was MAP (mm Hg) ≤ GA (wk).
authors.affiliation: Department of Neonatology, Copenhagen University Hospital-Rigshospitalet, Copenhagen, Denmark. gwhahn@dadlnet.dk
authors.forename: Gitte Holst
authors.initials: GH
authors.lastname: Hahn
authors.forename: Lisa L
authors.initials: LL
authors.lastname: Maroun
authors.forename: Nanna
authors.initials: N
authors.lastname: Larsen
authors.forename: David M
authors.initials: DM
authors.lastname: Hougaard
authors.forename: Line C
authors.initials: LC
authors.lastname: Sorensen
authors.forename: Hans C
authors.initials: HC
authors.lastname: Lou
authors.forename: Gorm
authors.initials: G
authors.lastname: Greisen
mesh_terms: D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D054022:Cerebrum / Q000502:physiology*; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D007022:Hypotension / Q000503:physiopathology; D007231:Infant, Newborn; D007249:Inflammation / Q000503:physiopathology*; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D047928:Premature Birth / Q000503:physiopathology*; D012189:Retrospective Studies
chemical_list: D015415:Biomarkers; D015850:Interleukin-6