ENDOTOXIN-INDUCED PULMONARY LEUKOSTASIS IN THE RAT - ROLE OF PLATELET-ACTIVATING-FACTOR AND TUMOR-NECROSIS-FACTOR

被引:0
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作者
CHANG, SW
机构
[1] NORTHWESTERN UNIV,SCH MED,DEPT MED,CHICAGO,IL 60611
[2] LAKESIDE MED CTR,DEPT VET AFFAIRS,CHICAGO,IL
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中图分类号
R446 [实验室诊断]; R-33 [实验医学、医学实验];
学科分类号
1001 ;
摘要
Injection of bacterial lipopolysaccharide (LPS) into experimental animals induces septic shock associated with the release of tumor necrosis factor (TNF) and platelet-activating factor (PAF). Because both TNF and PAF stimulate neutrophil adhesion to endothelial cells in vitro, and because neutrophils are important effector cells in sepsis-induced lung vascular injury, the role of TNF and PAF in LPS-induced lung neutrophil sequestration was investigated. Lung myeloperoxidase (MPG) activity was measured as a quantitative assessment of pulmonary leukostasis. Injection of Salmonella enteritidis LPS into rats caused dose-dependent increases in lung MPO that peaked at 2 hours and persisted for up to 24 hours. Injection of purified human recombinant TNF (2 to 200 mu g/kg IV) mimicked the effect of LPS on lung MPG activity. Injection of synthetic PAF increased lung MPO only at the highest and lethal dose (10 mu g/kg). Lower doses (0.1 and I mu g/kg) of PAF had no effect on lung MPG by itself and did not enhance LPS- or TNF-induced lung neutrophil sequestration. Furthermore, pretreatment of the rats with two different PAF receptor-antagonists, WEB 2086 (10 mg/kg IP) and SRI 63-441 (10 mg/kg IP), failed to block LPS-induced (I mg/kg) increase in lung MPO. These data suggest that TNF, not PAF, mediates LPS-induced pulmonary neutrophil sequestration in the intact rat.
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页码:65 / 72
页数:8
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