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Transient hyperoxia does not affect regional cerebral tissue oxygen saturation in moderately preterm or term newborns
Author(s) -
Thing Mira,
Sørensen Line Carøe,
Pryds Ole
Publication year - 2015
Publication title -
acta paediatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/apa.12860
Subject(s) - hyperoxia , medicine , vasoconstriction , anesthesia , gestational age , oxygen , ischemia , hypoxia (environmental) , cardiology , pregnancy , lung , chemistry , organic chemistry , biology , genetics
Aim Even 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 (rStO 2 ) and to evaluate whether any observed prolonged cerebral vasoconstriction was related to maturity. Methods The 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 rStO 2 before, during and after two hyperoxic exposures. If hyperoxia induced a prolonged cerebral vasoconstriction, posthyperoxic rStO 2 would be expected to decrease. Results rStO 2 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, rStO 2 remained unchanged with a mean difference of −0.4% (95% CI −1.6, 0.78). Differences in rStO 2 were not related to gestational age in either of the two hyperoxic episodes. Conclusion We found no evidence to support the theory that transient hyperoxia induces prolonged cerebral vasoconstriction in infants with a postmenstrual age above 32 weeks.