Comparison of Postasphyxial Resuscitation with 100% and 21% Oxygen on Cortical Oxygen Pressure and Striatal Dopamine Metabolism in Newborn Piglets

Abstract: The present study tests the hypothesis that ventilation with 100% O₂ during recovery from asphyxia leads to greater disturbance in brain function, as measured by dopamine metabolism, than does ventilation with 21% oxygen. This hypothesis was tested using mechanically ventilated, anesthetized newborn piglets as an animal model. Cortical oxygen pressure was measured by the oxygen‐dependent quenching of phosphorescence, striatal blood flow by laser Doppler, and the extracellular levels of dopamine and its metabolites by in vivo microdialysis. After establishment of a baseline, both the fraction of inspired oxygen (FiO₂) and the ventilator rate were reduced in a stepwise fashion every 20 min over a 1‐h period. For the subsequent 2‐h recovery, the animals were randomized to breathing 21 or 100% oxygen. It was observed that during asphyxia cortical oxygen pressure decreased from 36 to 7 torr, extracellular dopamine increased 8,300%, and dihydroxyphenylacetic acid and homovanillic acid decreased by 65 and 60%, respectively, compared with controls. During reoxygenation after asphyxia, cortical oxygen pressure was significantly higher in the piglets ventilated with 100% oxygen than in those ventilated with 21% oxygen (19 vs. 11 torr). During the first hour of reoxygenation, extracellular dopamine levels decreased to ∼200% of control in the 21% oxygen group, whereas these levels were still much higher in the 100% oxygen group (∼500% of control). After ∼2 h of reoxygenation, there was a secondary increase in extracellular dopamine to ∼750 and ∼3,000% of baseline for the animals ventilated with 21 and 100%, respectively. It is concluded that although 100% FiO₂ after asphyxia increases cortical oxygenation compared with 21% FiO₂, it also results in poorer recovery in dopamine metabolism and higher secondary release of striatal dopamine. The resulting increased extracellular levels of dopamine may exacerbate posthypoxic cerebral injury.