Endotoxin protection of rats from O2 toxicity: chemiluminescence of lung neutrophils.

Endotoxin (1 mg/kg body weight, I.P.) greatly reduces pulmonary permeability edema in rats breathing greater than 99% O2. Polymorphonuclear leukocytes (PMN's) have the potential to damage tissue by releasing free radicals or proteolytic enzymes and are needed to produce permeability edema in some models. This study evaluates the possibility that endotoxin protects rats from the pulmonary edema of O2 toxicity by inhibiting free radical release by lung PMN's. The potential of lavaged phagocytes to generate free radicals was determined using zymosan stimulated chemiluminescence (Cl). Values were then expressed as peak C1/10(6) PMN's. We found that PMN peak C1 fell progressively with time of O2 exposure. Peak C1 by PMN's from saline pretreated rats breathing O2 for 3 days was 80% lower than peak C1 by PMN's from paired rats pretreated with endotoxin. Assuming that peak C1 (measured in vitro) inversely reflects the level of free radical release by PMN's prior to lavage, the data suggest that endotoxin protects rats from O2 toxicity by inhibiting in vivo free radical release by lung PMN's.