In vitro effect of carprofen and meloxicam on the conductance and permeability to mannitol and the histologic appearance of the gastric mucosa of dogs

Hicks, Merrin; Hosgood, Giselle; Morgan, Timothy W.; Briere, Catherine A.; McConnico, Rebecca S.

doi:10.2460/ajvr.72.4.570

Cited by 3 publications

(2 citation statements)

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“…Additionally, barrier function can be assessed using flux of a larger molecule, such as mannitol or dextrans, which is radiolabeled or fluorescently tagged and can only move paracellularly. In dogs, this model system has been previously used to examine effects of carprofen and meloxicam . Using an ex vivo model of acid‐induced gastric barrier dysfunction, we sought to investigate the effect of the parent compound tramadol on gastric barrier function as well as its potential interaction with a nonselective COX inhibitor, indomethacin.…”

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“…In dogs, this model system has been previously used to examine effects of carprofen and meloxicam. 7 Using an ex vivo model of acid-induced gastric barrier dysfunction, we sought to investigate the effect of the parent compound tramadol on gastric barrier function as well as its potential interaction with a nonselective COX inhibitor, indomethacin. We hypothesized that tramadol would have an additive or synergistic effect with a nonselective COX inhibitor, indomethacin, in decreasing recovery of barrier function, as assessed by transepithelial resistance and 3 H-mannitol flux, after injury.…”

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The Effect of Tramadol and Indomethacin Coadministration on Gastric Barrier Function in Dogs

Hill

Lascelles

Law

et al. 2014

Veterinary Internal Medicne

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BackgroundTramadol is a centrally acting analgesic that is often used in conjunction with nonsteroidal anti‐inflammatory drugs (NSAIDs). The effect of coadministration of tramadol and indomethacin on gastric barrier function in dogs is unknown.Hypothesis/ObjectivesThat coadministration of a nonselective NSAID (indomethacin) and tramadol would decrease recovery of barrier function as compared with acid‐injured, indomethacin‐treated, and tramadol‐treated mucosa.AnimalsGastric mucosa of 10 humanely euthanized shelter dogs.MethodsEx vivo study. Mounted gastric mucosa was treated with indomethacin, tramadol, or both. Gastric barrier function, prostanoid production, and cyclooxygenase expression were quantified.ResultsIndomethacin decreased recovery of transepithelial electrical resistance after injury, although neither tramadol nor the coadministration of the two had an additional effect. Indomethacin inhibited production of gastroprotective prostanoids prostaglandin E2 (acid‐injured PGE 2: 509.3 ± 158.3 pg/mL, indomethacin + acid injury PGE 2: 182.9 ± 93.8 pg/mL, P < .001) and thromboxane B2 (acid‐injured TXB 2: 233.2 ± 90.7 pg/mL, indomethacin + acid injury TXB 2: 37.9 ± 16.8 pg/mL, P < .001), whereas tramadol had no significant effect (PGE 2 P = .713, TXB 2 P = .194). Neither drug had an effect on cyclooxygenase expression (COX‐1 P = .743, COX‐2 P = .705). Acid injury induced moderate to marked epithelial cell sloughing, which was unchanged by drug administration.Conclusions and Clinical ImportanceThere was no apparent interaction of tramadol and a nonselective cyclooxygenase in this ex vivo model. These results suggest that if there is an adverse interaction of the 2 drugs in vivo, it is unlikely to be via prostanoid inhibition.

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confidence: 99%