Hyperoxia effects on lung vascular circulating and marginated leukocytes in the rat.
The vascular sequestration of polymorphonuclear leukocytes (PMN) may be responsible for endothelial injury leading to lung oedema, which occurs when rats are exposed to pure normobaric oxygen. Indeed, marginated PMN in close contact with the endothelium are able to damage the latter when activated. In the present work, marginated leukocytes were recovered by lavage through the pulmonary artery in isolated rat lung and the leukocyte differential count in blood and in the lung perfusion liquid (perfusate) was studied. Following 55 h of hyperoxia, a rise in the PMN count and lymphocytopenia were observed in the blood and in the perfusate. Moreover, the relatively greater increase in the PMN concentration in the perfusate than in the blood suggested a strengthening of their margination along the endothelium. A clear protective effect was noted during hyperoxia provided previous injection of endotoxin (1.5 mg X kg-1 intraperitoneally) had been performed. Indeed, after 65 h of hyperoxia, none of these rats (Endo/O2) died and there was no pleural effusion. The lymphocyte count was maintained within the normal limit and the number of PMN in the lung perfusion fluid and in blood was reduced. Results of this study suggest an essential role of the marginated PMN in lung oxygen toxicity.
D000818:Animals; D004731:Endotoxins / Q000494:pharmacology; D004926:Escherichia coli; D007958:Leukocyte Count / Q000187:drug effects; D008168:Lung / Q000098:blood supply* / Q000187:drug effects; D008297:Male; D009504:Neutrophils / Q000502:physiology*; D010100:Oxygen / Q000494:pharmacology*; D010477:Perfusion; D011651:Pulmonary Artery / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains
D004731:Endotoxins; D010100:Oxygen