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Abstract

Objectives: Critically ill patients often require mechanical ventilatory support and increased inspiratory 0 2 concentration. Experimentally, continuous breathing of 100% 02 in animals leads to progressive irreversible damage to the lung, ARDS and death. In critical care units 100% 0 2 is often administered for several hours. The mechanism of hyperoxia induced lung injury is unclear. The objective of this study is to explore inflammatory mediator responses following breathing 100% 0 2 in humans. Ten healthy subjects aged 32-46 breathed 100% 0 2 for 60 minutes. Minute ventilation, arterial 02 saturation, blood pressure, heart rate and EKG were continually monitored. Methods: Interleukin-1 beta (IL-1(3) and Interleukin-1 receptor antagonist (IL-ira) were determined by ELISA in the supernatant of whole blood incubated with Endotoxin by the method of Nerad and Dinarello, before (To), at the end of 60 minutes of 100% Oz breathing (F6o) and at 90 (Tso) and 180 (Ttso) minutes following resumption of air breathing. Results: pg/ml 02 Breathing Air Breathing To