mobic and Vomiting

A female, mixed-breed dog was presented with signs of abdominal discomfort and vomiting of 24 h duration following an episode of dietary indiscretion. Clinical signs, previous medical history, and diagnostic tests supported a diagnosis of acute pancreatitis. Specific and supportive treatment was instituted, and clinical signs resolved 10 d after presentation.

Topics: Acute Disease; Animal Feed; Animals; Anti-Inflammatory Agents, Non-Steroidal; Blood Cell Count; Dehydration; Dog Diseases; Dogs; Female; Medical History Taking; Meloxicam; Pancreatitis; Quinuclidines; Radiography; Tachycardia; Thiazines; Thiazoles; Treatment Outcome; Vomiting

The objective of this study was to investigate the metabolic pathways and routes of excretion of oral meloxicam in the cat. [(14)C]-meloxicam was administered orally to three fasted male cats. Urine, faeces, vomit and cage washes were collected over the following 144 h period. Blood was collected predosing and at 3 and 12 h postdosing. Metabolites were identified by HPLC/MS/MS. When possible a metabolic structure was proposed for each metabolite detected. Only unchanged meloxicam was identified in plasma. Five major metabolites were detected in urine and four in faeces, which were identified by HPLC/MS/MS as products of oxidative metabolism. No conjugated metabolites were detected. Elimination occurred early (61% during the first 48 h). A total of 21% of the recovered dose was eliminated in urine (2% as unchanged meloxicam, 19% as metabolites) and 79% in the faeces (49% as unchanged meloxicam, 30% as metabolites). The results indicate that after oral administration the major route of excretion of meloxicam in the cat is faecal and that the main pathway of biotransformation of meloxicam in the cat is oxidation.

Topics: Administration, Oral; Animals; Anti-Inflammatory Agents, Non-Steroidal; Carbon Radioisotopes; Cats; Chromatography, High Pressure Liquid; Feces; Male; Meloxicam; Thiazines; Thiazoles; Vomiting

We analysed the effects of four cyclooxygenases (COX) inhibitors on cisplatin-induced emesis in piglets. Ninety-five animals receiving cisplatin (5.5 mg kg(-1), i.v.) were observed for 60 h. One hour prior to cisplatin, controls (n=29) were dosed with a saline solution while experimental animals received an i.v. or i.p. injection of one of the COX inhibitors. Additional injections of COX inhibitor were given at 15 and 39 h after cisplatin administration (or every 6h in one group receiving diclofenac). The latencies to the first emetic episode (EE) compared to controls (2.1+/-0.4 h) increased in groups receiving naproxen (4.66+/-0.94 h, n=9, 30 mg kg(-1)) and indomethacin (6.19+/-1.13 h, n=7, 10 mg kg(-1)) i.v. Indomethacin significantly decreased the incidence of both the acute (by 40%) and delayed (by 66%) phases of emesis. The total number of EE during the 60 h compared to controls (28.3+/-1.9 EE) was significantly reduced in piglets receiving indomethacin (14.9+/-3.2 EE, n=7) and meloxicam (17.6+/-3.6 EE, n=11, 0.3 mg kg(-1)). Four piglets receiving meloxicam (0.3 mg kg(-1), i.v.) did not vomit during the delayed phase. The anti-emetic activity of two COX inhibitors suggests that prostaglandins contribute to the activation of the emetic reflex in response to cisplatin.

Topics: Animals; Antiemetics; Antineoplastic Agents; Cisplatin; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Female; Indomethacin; Isoenzymes; Male; Meloxicam; Prostaglandin-Endoperoxide Synthases; Swine; Thiazines; Thiazoles; Vomiting

The emetic response to intraperitoneal (i.p., 0.5, 2, 8 mg kg(-1)) and intravenous (i.v., 200 microg kg(-1)) administration of bacterial lipopolysaccharides (LPS) was characterized in conscious piglets observed for 4 h. The latencies and the incidence of the emetic response to LPS (i.p.) decreased and increased, respectively, in a dose-dependent manner. In 14 additional piglets, a bilateral vagotomy performed 4 h prior to LPS administration abolished the vomiting induced by i.p. LPS (2 mg kg(-1)), and decreased its incidence by 77% in the i.v. injected animals. Sham-operated animals (n=6) exhibited a similar emetic pattern to the controls injected intraperitoneally with LPS (2 mg kg(-1)). In 7 piglets, the administration of granisetron, a 5-HT(3) receptor antagonist (i.v., 2 mg kg(-1)), 30 min prior to the i.p. LPS injection (2 mg kg(-1)) failed to reduce significantly the emetic activity; whereas, in 6 animals, a combination of meloxicam (0.3 mg kg(-1)) and indomethacin (5 mg kg(-1)), two cyclooxygenase (COX) inhibitors, administered per os 1.5 h prior to the i.p. LPS (2 mg kg(-1)) abolished the emetic response to endotoxins. The present results show that the activation of the medullary "vomiting centre" in response to i.p. administration of LPS is mediated via vagal afferents and is likely to involve prostaglandins.

Topics: Animals; Antiemetics; Behavior, Animal; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dose-Response Relationship, Drug; Granisetron; Indomethacin; Injections, Intraperitoneal; Isoenzymes; Lipopolysaccharides; Meloxicam; Prostaglandin-Endoperoxide Synthases; Receptors, Serotonin; Receptors, Serotonin, 5-HT3; Serotonin Antagonists; Sick Role; Swine; Thiazines; Thiazoles; Vagotomy; Vomiting