Endocrine, metabolic and clinical effects of intravenous endotoxin injection after pre-treatment with meloxicam in heifers.

Meloxicam (M), a non-steroid anti-inflammatory drug for use in animals, reduces prostaglandin (PG) synthesis by inhibiting cyclooxygenases-1 and -2. The aim of this study was to evaluate M's capability to prevent the inflammatory response elicited by endotoxin (ET). Furthermore, we wanted to evaluate a possible effect of M on delta13-reductase and 15-hydroxy prostanoate dehydrogenase, enzymes responsible for the initial metabolism of PGF2alpha. Four heifers acting as their own controls were used in the study. The heifers received an i.v. injection of either saline (S) or M (0.5 mg/kg) at 1.5 h before an i.v. injection of ET (50 ng/kg b.w. i.v.). The trial lasted 57 h after ET injection and blood samples were withdrawn for analyses of 15-ketodihydro-PGF2alpha (PG metabolite), cortisol, white blood cells (WBC), Fe, Zn and Ca. Clinical examinations were performed throughout the trial. In the S + ET trial, ET injection elicited a rapid increase of the PG metabolite, a prolonged cortisol release and reduced levels of WBC, Fe, Zn and Ca. General appearance and body temperature were affected. In the M + ET trial the PG release was totally abolished, the cortisol release was reduced and the clinical effect was milder, also effects on Fe, Zn and Ca were milder in the M + ET trial, but M did not prevent the pyrogenic effect of ET. In the next two trials, we injected PGF2alpha (500 ng/kg i.v.) with and without M pre-treatment. After PGF2alpha injection, plasma samples were collected for measurement of the PG metabolite. M had no effect on PGF2alpha metabolism. In conclusion, M effectively suppresses several of the inflammatory reactions seen after ET injections and has no major influence on the PGF2alpha metabolism.