Impaired early neurologic outcome in newborn piglets reoxygenated with 100% oxygen compared with room air after pneumothorax-induced asphyxia

Birth asphyxia is a serious problem worldwide, resulting in 1 million death s and an equal number of neurologic sequelae annually, It is therefore impo rtant to develop new and better ways to treat asphyxia. In the present stud y we tested the effects of reoxygenation with room air or with 100% oxygen (O-2 after experimental pneumothorax-induced asphyxia on the blood oxidativ e stress indicators, early neurologic outcome, and cerebral histopathology of newborn piglets. Twenty-six animals were studied in three experimental g roups: I) sham-operated animals (SHAM, n = 6), 2) animals reoxygenated with room air after pneumothorax (R2I, n = 10), and 3) animals reoxygenated wit h 100% O-2 after pneumothorax (R100, n = 10), In groups R21 and R100, asphy xia was induced under anesthesia with bilateral intrapleural room air insuf flation, Gasping, bradyarrhythmia, arterial hypotension, hypoxemia, hyperca rbia, and combined acidosis occurred 62 +/- 6 min (R21) or 65 +/- 7 min (R1 00; mean C SD) after the star? of the experiments; then pneumothorax was re lieved, and a 10-min reoxygenation period was started with mechanical venti lation with room air (R21) or with 100% O-2 (R100). The newborn piglets the n breathed room air spontaneously during the next 3 h. Blood oxidative stre ss indicators (oxidized and reduced glutathione, plasma Hb, and malondialde hyde concentrations) were measured at different stages of the experiments. Early neurologic outcome examinations (neurologic score of 20 indicates nor mal, 5 indicates brain-dead) were performed at the end of the study. The br ains were next fixed, and various regions were stained for cerebral histopa thology. In the SHAM group, the blood gas and acid-base status differed sig nificantly from those measured in groups R21 and R100. In group R100, arter ial Po-2 was significantly higher after 5 (13.8 +/- 5.6 kPa) and 10 min (13 .2 +/- 6.3 kPa) of reoxygenation than in group R21 (8.7 +/- 2.5 kPa and 9.2 +/- 3.1 kPa). The levels of all oxidative stress indicators remained uncha nged in the study groups (SHAM, R21, and R100). The neurologic examination score in the SHAM group was 18 +/- 0, in group R21 it was 13.5 +/- 3.1, and in group R100 it was 9.5 +/- 4.1 (significant differences between SHAM and R21 or R100, and between R21 and R100). Cerebral histopathology revealed m arked damage of similar severity in both asphyxiated groups. We conclude th at the blood oxidative stress indicators and cerebral histopathology did no t differ significantly after a 10-min period of reoxygenation with room air or with 100% O-2 after pneumothorax-induced asphyxia, but reoxygenation wi th 100% O-2 might impair the early neurologic outcome of newborn piglets.