作者: J. A. Cook , W. C. Wise , P. V. Halushka
DOI: 10.1172/JCI109655
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摘要: The potential deleterious role of the proaggregatory vasoconstrictor, thromboxane A(2), in endotoxic shock was investigated rats. Plasma A(2) determined by radioimmunoassay its stable metabolite B(2). After intravenous administration Salmonella enteritidis endotoxin (20 mg/kg), plasma B(2) levels increased from nondetectable (<375 pg/ml) normal control rats to 2,054+/-524 pg/ml (n = 8), within 30 min 2,071+/-429 at 60 min, and decreased 1,119+/-319 pg/ml, 120 min. prostaglandin E also 146+/-33 controls 5) 2,161+/-606 after 5). In contrast shocked controls, pretreated with imidazole, a synthetase inhibitor, or essential fatty acid-deficient rats, which are deficient arachidonate metabolites, did not exhibit significant elevations Imidazole however inhibit endotoxin-induced E. Essential acid deficiency significantly reduced mortality lethal shock. This refractoriness could be duplicated cyclo-oxygenase indomethacin (10 intravenously before injection. (30 mg/kg) administered intraperitoneally 1 h endotoxin, (P < 0.01) 40% compared 95% 24 h. Likewise pretreatment 13-azaprostanoic antagonist, 100% only 50% 0.01). results suggest that induces synthesis may contribute pathogenesis