Transient Hyperoxia and Residual Cerebrovascular Effects in the Newborn Rat

Unrestricted use of oxygen in the delivery room after preterm birth has been associated with reduced cerebral blood flow (CBF) 2 h later. To further investigate residual cerebrovascular effects of transient hyperoxia, we developed a newborn rat model in which laser-Doppler flowmetry (LDF) and near-infrared spectroscopy (NIRS) were used to monitor changes in cerebral perfusion. The hypothesis to be tested was that hyperoxic exposure limits cerebral vasodilation in response to increase in carbon dioxide tension (Pco2). Twenty-four 3- to 5-d-old rats were kept on spontaneous breathing with doxapram under light isoflurane anesthesia, randomized into two groups, and exposed to either room air or 100% oxygen for 30 min. Then, after 15 min of stabilization in normoxia, 8% CO2 was given for 5 min. No significant differences in CO2 responses were observed between the two groups: mean CBF-CO2 reactivity as measured by NIRS was 13.3 ± 3.9 %/kPa in the normoxia-group versus 8.8 ± 4.1 %/kPa in the hyperoxia group (NS). The oxygenation index [(HbO2 - Hb)/2] increased by 0.67 ± 0.17 μmol/L/kPa in the normoxia group compared with 1.18 ± 0.19 μmol/L/kPa in the hyperoxia group (NS). Cortical perfusion, monitored by LDF, increased by 7.3 ± 1.5 %/kPa versus 6.8 ± 1.8 %/kPa in the normoxia and hyperoxia groups, respectively (NS). We conclude that in newborn rats the CBF-CO2 reactivity remains intact after 30 min of oxygen exposure.