COMPARISON OF POSTASPHYXIAL RESUSCITATION WITH 100-PERCENT AND 21-PERCENT OXYGEN ON CORTICAL OXYGEN-PRESSURE AND STRIATAL DOPAMINE METABOLISM IN NEWBORN PIGLETS

The present study tests the hypothesis that ventilation with 100% O-2 during recovery from asphyxia leads to greater disturbance in brain fu nction, 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 pres sure was measured by the oxygen-dependent quenching of phosphorescence , striatal blood flow by laser Doppler, and the extracellular levels o f dopamine and its metabolites by in vivo microdialysis. After establi shment of a baseline, both the fraction of inspired oxygen (FiO(2)) an d 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 r andomized to breathing 21 or 100% oxygen. It was observed that during asphyxia cortical oxygen pressure decreased from 36 to 7 torr, extrace llular dopamine increased 8,300%, and dihydroxyphenylacetic acid and h omovanillic acid decreased by 65 and 60%, respectively, compared with controls. During reoxygenation after asphyxia, cortical oxygen pressur e 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 t o similar to 200% of control in the 21% oxygen group, whereas these le vels were still much higher in the 100% oxygen group (similar to 500% of control). After similar to 2 h of reoxygenation, there was a second ary increase in extracellular dopamine to similar to 750 and similar t o 3,000% of baseline for the animals ventilated with 21 and 100%, resp ectively. It is concluded that although 100% FiO(2) after asphyxia inc reases cortical oxygenation compared with 21% FiO(2), 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.