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Korean J Crit Care Med > Volume 14(2); 1999 > Article
Korean Journal of Critical Care Medicine 1999;14(2): 137-142.
흰쥐에서 내독소 투여가 유발하는 생리학적 변화
이경민, 이광호, 임공빈, 박종택, 이영복
연세대학교 원주의과대학 마취과학교실
Physiologic Changes Induced with Lipopolysaccharide in Rats
Kyoung Min Lee, Kwang Ho Lee, Kong Been Im, Jong Taek Park, Young Bok Lee
Department of Anesthesiology and Critical Care Medicine, Yonsei University, Wonju College of Medicine, Wonju, Korea.
ABSTRACT
BACKGOUND: Bacterial endotoxin or lipopolysaccharide (LPS) is believed to mediate the tissue damage and shock observed in Gram-negative sepsis (GNS) by initiating a cascade of events, including activation of the coagulation, fibrinolytic and complement systems, and release of proinflammatory cytokines. However, the clinical pictures that result from GNS and endotoxin are quite different. The physiologic changes induced with LPS were investigated in this study. METHODS: Fifty two male Sprague-Dawley rats were injected intraperitoneally with Escherichia coli LPS. Blood samples and bronchoalveolar lavage (BAL) fluid were obtained at baseline and at 2, 4, 8, 16, 24, and 48 hours after injection. Nitrate/nitrite levels were measured from plasma and BAL samples. Lipid peroxide (LPO) levels were measured from plasma. We measured also protein concentration and number of polymorphonuclear leukocytes (PMNL) and macrophages from BAL samples. RESULTS: Administration of LPS caused significant increase in nitrate/nitrite concentrations of plasma and BAL fluid (p<0.01). ED50 of LPS was 1.76 mg/kg in plasma nitrate/nitrite assay. Plasma LPO levels were increased slightly after administration of LPS, but no statistical significance. Protein concentration was increased significantly (p<0.01) 4 hours after the administration of LPS. LPS induced increase of the number of PMNLs and macrophages of BAL samples significantly (p<0.05). CONCLUSIONS: LPS increased NO production and alveolar permeability in rats. Also, LPS increased the number of inflammatory cells in the lung.
Key Words: Pharmacology; Lipopolysaccharide; Nitric oxide; Sepsis
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