Cerebral autoregulation in the first day after preterm birth: no evidence of association with systemic inflammation

Gitte Holst Hahn, Lisa L Maroun, Nanna Brink Larsen, David M Hougaard, Line C Sorensen, Hans C Lou, Gorm Greisen

    18 Citationer (Scopus)

    Abstract

    Introduction: 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). Discussion: 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).

    OriginalsprogEngelsk
    TidsskriftPediatric Research
    Vol/bind71
    Udgave nummer3
    Sider (fra-til)253-60
    Antal sider8
    ISSN0031-3998
    DOI
    StatusUdgivet - mar. 2012

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