Pathophysiology of experimental bovine endotoxicosis: endotoxin induced synthesis of prostaglandins and thromboxane and the modulatory effect of some non-steroidal anti-inflammatory drugs

• Published in: Acta veterinaria scandinavica Vol. 33; no. 1; pp. 1 - 8
• Main Authors: Jarløv, N, Andersen, P H, Hesselholt, M
• Format: Journal Article
• Language: English
• Published: England BioMed Central 01-03-1992
• Subjects: Animals; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use; Cattle; Cattle Diseases - chemically induced; Cattle Diseases - drug therapy; Cattle Diseases - physiopathology; Endotoxins - toxicity; Escherichia coli; Female; Prostaglandins - biosynthesis; Thromboxane A2 - biosynthesis
• ISSN: 0044-605X; 1751-0147; 1751-0147
• DOI: 10.1186/BF03546929

Endotoxin-induced synthesis of thromboxane A2 (TXA2), prostacyclin (PGI2) and prostaglandin E2 (PGE2) was studied in 3 cows after intravenous E. coli endotoxin (055:B5-0.025 mg/kg b.w.) administration. Blood sampling and monitoring of clinical signs were performed from 2 h prior to until 6 h after endotoxin challenge. Blood samples were analyzed for stable hydrolysis products of TXA2 (TXB2), PGI2 (6-keto PGF) and PGE2 (bicyclic PGE2), biochemical and haematological parameters. In a similar experimental design the efficacy of the non-steroidal anti-inflammatory drugs (NSAID) flunixin meglumine (FM) and phenylbutazone (PB) in suppressing eicosanoid synthesis and clinical signs in response to endotoxin challenge was investigated. Two groups of cows, each comprising 2 animals, were treated with FM and PB prior to endotoxin challenge. It was observed that plasma concentrations of TXB2, 6-keto PGF and bicyclic PGE2 increased rapidly after endotoxin challenge. Concentrations were significantly elevated for hours and were correlated to the severity of clinical signs of endotoxicosis. Pretreatment with NSAID suppressed mediator production and alleviated clinical signs. The experiments suggest a certain pathophysiological role of TXA2, PGI2 and PGE2 for the early systemic ill-effects of bovine endotoxicosis.