Reversible Pulmonary Oxygen Toxicity in the Primate

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Abstract

In order to investigate the effects of high concentrations of oxygen on the lung, experiments were performed on 18 baboons exposed to a humidified environment of 95% oxygen for five days. Open lung biopsies for biochemical assay, histologic and electron microscopic analysis and measurement of tissue respiration were performed before and after oxygen exposure. Pulmonary function was evaluated by measurement of arterial blood gases, compliance, closing capacity (CC), functional residual capacity (FRC), total lung capacity (TLC), residual volume (RV) and vital capacity (VC) before and after exposure and then at seven and 14 days in the animals which recovered. Six baboons removed from the oxygen environment after 96–110 hours and exposed to room air died within three to 20 hours of profound hypoxemia (Pao2 40 ± 6). The remaining 12 baboons were successfully weaned to room air over a three day period with a return of ABGs to control values (Pao2 89 ± 2). Electron microscopic analysis of alveolar membranes exposed to 120 hours of hyperoxia demonstrated endothelial cell swelling, interstitial alveolar membrane edema, and an increased predominance of Type II pneumocytes. Lung volume measurements showed significant decreases in TLC (25%), VC (34%), CC/TLC (28%) and dynamic compliance (47%). Biochemical studies indicated a shift toward anaerobic metabolism with a decrease in tissue oxygen consumption, reduced cytochrome oxidase activity, and increased lung lactic acid production. These changes were all found to be reversible in the 12 baboons slowly weaned back to room air

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