Inhibition by terbutaline of nitric oxide and superoxide anion levels of endotoxin-induced organs injury in the anesthetized rat
Autor: | Shiu Jen Chen, Chin-Chen Wu, Jih Hsin Wang, Jeng Yuan Wu, Wen Jinn Liaw, Chin Tzao |
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Rok vydání: | 2003 |
Předmět: |
Lipopolysaccharides
Male medicine.medical_specialty Lipopolysaccharide Terbutaline Inflammation Blood Pressure Critical Care and Intensive Care Medicine Nitric Oxide Rats Inbred WKY Nitric oxide Proinflammatory cytokine chemistry.chemical_compound Superoxides Internal medicine medicine Animals Septic shock business.industry Superoxide Tumor Necrosis Factor-alpha Hemodynamics medicine.disease Shock Septic Rats Endotoxins Kinetics Endocrinology chemistry Immunology Emergency Medicine Tumor necrosis factor alpha medicine.symptom business medicine.drug |
Zdroj: | Shock (Augusta, Ga.). 19(3) |
ISSN: | 1073-2322 |
Popis: | Despite the fact that septic shock is characterized by a decrease in systemic vascular resistance, the main cause of death is due to multiple organ failure. The organ dysfunction is usually attributed to cell death caused by overproduction of free radicals derived from inflammation. In the host infected by endotoxin (lipopolysaccharide, LPS), the expression and release of proinflammatory tumor necrosis factor-alpha (TNF-alpha) rapidly increases, and the formation of free radicals (e.g., superoxide anion [O2*-] and nitric oxide [NO*] in the present study) are inevitably overproduced. In this study, we present evidence that overall treatment of LPS rats with terbutaline, a beta2-adrenoceptor agonist, attenuates the delayed hypotension and ameliorates the tachycardia. Overproduction of TNF-alpha and NO* (produced by inducible NO synthase [iNOS] examined by Western blot analysis in the lung and the liver) is inhibited by treatment of LPS rats with terbutaline. In addition, treatment of endotoxemic rats with terbutaline also reduces the O2*- levels in the lung and the liver. Terbutaline also improves the liver (assessed by aspartate aminotransferase, alanine aminotransferase, total bilirubin, and albumin/globulin) and kidney (assessed by creatinine and uric acid) dysfunction induced by endotoxin. These findings suggest that the amelioration of circulatory failure and organs injury by terbutaline is associated with its suppression in TNF-alpha, O2*- and NO (via iNOS) production in animals with endotoxic shock. |
Databáze: | OpenAIRE |
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