Modulation of arachidonic acid metabolism in endotoxic horses: Comparison of flunixin meglumine, phenylbutazone, and a selective thromboxane synthetase inhibitor

• Published in: American journal of veterinary research Vol. 47; no. 1; p. 110
• Main Authors: Moore, J.N, Hardee, M.M, Hardee, G.E
• Format: Journal Article
• Language: English
• Published: United States 01.01.1986
• Subjects: 6-Ketoprostaglandin F1 alpha - blood; ACIDE GRAS; ACIDOS GRASOS; ANALGESICOS; ANALGESICS; ANALGESIQUE; Animals; Arachidonic Acid; Arachidonic Acids - metabolism; CABALLOS; CHEVAL; Clonixin - analogs & derivatives; Clonixin - pharmacology; endotoxemia; ENDOTOXINAS; ENDOTOXINE; ENDOTOXINS; Endotoxins - administration & dosage; Endotoxins - blood; Escherichia coli; FATTY ACIDS; HORSES; Imidazoles - pharmacology; Lactates - blood; Male; METABOLISM; METABOLISME; METABOLISMO; Nicotinic Acids - pharmacology; Phenylbutazone - pharmacology; Thromboxane B2 - blood; Thromboxane-A Synthase - antagonists & inhibitors; THROMBOXANES
• ISSN: 0002-9645; 1943-5681

Two cyclooxygenase inhibitors (flunixin meglumine and phenylbutazone) and a selective thromboxane synthetase inhibitor were assessed in the management of experimental equine endotoxemia. Drugs or saline solution were administered to 16 horses 15 minutes before administration of a sublethal dose of endotoxin (Escherichia coli 055:B5). Plasma concentrations of thromboxane B2 (TxB2), prostacyclin (6-keto PGF1 alpha), plasma lactate, and hematologic values and clinical appearance were monitored for 3 hours after endotoxin administration. Pretreatment with flunixin meglumine (1 mg/kg of body weight) prevented most of the endotoxin-induced changes and correlated with a significant decrease in plasma TxB2 and 6-keto PGF1 alpha concentrations, compared with concentrations in nontreated horses (ie, pretreated with saline solution). Pretreatment with phenylbutazone (2 mg/kg) attenuated the effects of endotoxin and was associated with a brief, early, significant increase in plasma TxB2 concentrations, but not in plasma 6-keto PGF1 alpha concentrations. Pretreatment with the thromboxane synthetase inhibitor did not appear to clinically benefit the horses involved; however, arachidonic acid metabolism was redirected to prostacyclin production.