Oxygen toxicity in the premature baboon with hyaline membrane disease

R. A. Delemos, J. J. Coalson, D. R. Gerstmann, T. J. Kuehl, D. M. Null

Research output: Contribution to journalArticlepeer-review

61 Scopus citations

Abstract

Immaturity, pulmonary barotrauma, and oxygen toxicity have been implicated in the pathogenesis of bronchopulmonary dysplasia (BPD). Although the physiologic and biochemical consequences of oxygen toxicity have been described in newborn and adult animals, there have been no controlled observations in prematures. We compared the physiologic and morphologic effects of prolonged hyperoxia with those of clinically appropriate oxygen in premature baboons with hyaline membrane disease (HMD) supported with conventional positive pressure ventilation and continuous distending airway pressure (PPV/PEEP). Twenty-one premature baboons were delivered at 140 days gestation, intubated and resuscitated, and supported with PPV/PEEP and standard NICU techniques for 11 days. The FI(O2), Pa(O2), Pa(CO2), pHa, ventilator and airway pressures, and blood pressure were intermittently measured and recorded. The physiologic observations could be divided into 3 distinct phases. During Phase 1 (0 to 42 h) there were no significant intergroup differences, and (a/A)P(O2) and IO2 (oxygenation index; (a/A)P(O2)/P̄aw) remained stable. In Phase 2 (43 to 96 h) there was a rapid improvement in (a/A)P(O2) and IO2 in both groups, but the response in the hyperoxic animals was significantly dampened. During Phase 3 (97 to 264 h) there was continued improvement in the 'prn' animals, which contrasted with progressive deterioration in those exposed to FI(O2) 1.0. Five of 11 'prn' and 3 of 10 FI(O2) 1.0 baboons developed air leaks during Phase 1 or early Phase 2. Four of 10 of the hyperoxic animals died after the late onset of air leak. Pathologic changes of BPD were found in all FI(O2) 1.0 animals surviving more than 6 days but in none of the 'prn' long-term survivors. These data suggest that oxygen toxicity in the premature with HMD results in additive parenchymal injury, which prolongs the period of high risk for barotrauma. Both barotrauma and oxygen injury contribute to BPD in the premature baboon with HMD.

Original languageEnglish (US)
Pages (from-to)677-682
Number of pages6
JournalAmerican Review of Respiratory Disease
Volume136
Issue number3
DOIs
StatePublished - Jan 1 1987

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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