• Mira Thing, Line Carøe Sørensen, and Ole Pryds.
• Department of Paediatrics, Copenhagen University Hospital, Hvidovre, Denmark.
• Acta Paediatr. 2015 Jul 1; 104 (7): 657-62.

AimEven short periods of hyperoxia may induce prolonged cerebral vasoconstriction in newborn infants, and this could theoretically lead to cerebral ischaemia even once normoxia is re-established. This study aimed to investigate the effect of brief hyperoxic exposures on regional cerebral tissue oxygen saturation (rStO2 ) and to evaluate whether any observed prolonged cerebral vasoconstriction was related to maturity.MethodsThe study included 30 infants with a postmenstrual age of more than 32 weeks, who were treated with nasal continuous positive airway pressure and a fraction of inspired oxygen of ≤0.3. The INVOS 5100C oximeter was used to measure rStO2 before, during and after two hyperoxic exposures. If hyperoxia induced a prolonged cerebral vasoconstriction, posthyperoxic rStO2 would be expected to decrease.ResultsrStO2 increased slightly after the first hyperoxic exposure, with a mean difference of 1.37% (95% CI 0.15, 2.6). After the second oxygen exposure, rStO2 remained unchanged with a mean difference of -0.4% (95% CI -1.6, 0.78). Differences in rStO2 were not related to gestational age in either of the two hyperoxic episodes.ConclusionWe found no evidence to support the theory that transient hyperoxia induces prolonged cerebral vasoconstriction in infants with a postmenstrual age above 32 weeks.©2014 Foundation Acta Paediatrica. Published by John Wiley & Sons Ltd.

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