In vitro effects of cyclooxygenase inhibitors in whole blood of horses, dogs, and cats

Brideau, Christine; C, Van Staden; Chan, CC

doi:10.2460/ajvr.2001.62.1755

Cited by 179 publications

(196 citation statements)

References 20 publications

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“…Arterial blood pressure should be monitored and maintained within a normal range during anesthesia when carprofen or meloxicam are administered with butorphanol as premedication for dogs. Both clinical doses of carprofen and meloxicam provide effective postoperative analgesia when preoperatively administered [17][18][19], although meloxicam has higher in vitro selectivity of COX-2 inhibition than carprofen in dogs [5,15]. We also did not find any difference in sevofluranesparing effect between the treatments with carprofen alone and meloxicam alone, and between carprofen with butorphanol and meloxicam with butorphanol in dogs.…”

Section: Discussioncontrasting

confidence: 49%

“…NSAIDs are classified depending on the activity of each isoform as nonselective COX inhibitors and COX-2 selective inhibitors [6]. Carprofen and meloxicam are COX-2 selective inhibitors that have been shown to produce analgesic effects with minimal side effect in dogs [5,6,15,34]. Their preoperative administration to dogs undergoing ovariohysterectomy has been reported to produce a greater analgesic effect in the early postoperative period than does postoperative administration [18,19].…”

Section: Discussionmentioning

confidence: 99%

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Effects of Carprofen and Meloxicam with or without Butorphanol on the Minimum Alveolar Concentration of Sevoflurane in Dogs

et al. 2008

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ABSTRACT. Sparing effects of carprofen and meloxicam with or without butorphanol on the minimum alveolar concentration (MAC) of sevoflurane were determined in 6 dogs. Anesthesia was induced and maintained with sevoflurane in oxygen, and MAC was determined by use of a tail clamp method. The dogs were administered a subcutaneous injection of carprofen (4 mg/kg) or meloxicam (0.2 mg/kg), or no medication (control) one hour prior to induction of anesthesia. Following the initial determination of MAC, butorphanol (0.3 mg/ kg) was administered intramuscularly, and MAC was determined again. The sevoflurane MACs for carprofen alone (2.10 ± 0.26%) and meloxicam alone (2.06 ± 0.20%) were significantly less than the control (2.39 ± 0.26%). The sevoflurane MACs for the combination of carprofen with butorphanol (1.78 ± 0.20%) and meloxicam with butorphanol (1.66 ± 0.29%) were also significantly less than the control value after the administration of butorphanol (2.12 ± 0.28%). The sevoflurane sparing effects of the combinations of carprofen with butorphanol and meloxicam with butorphanol were additive.

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Section: Discussioncontrasting

confidence: 49%

Section: Discussionmentioning

confidence: 99%

Effects of Carprofen and Meloxicam with or without Butorphanol on the Minimum Alveolar Concentration of Sevoflurane in Dogs

et al. 2008

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“…* Ratio of IC50 for COX-1 to IC50 for COX-2 (positively correlated with COX-2 selectivity such that a ratio < 1 indicates COX-1 selectivity and a ratio > 1 indicates COX-2 selectivity). Based on references [33][34][35][36] Biochem Pharmacol. Author manuscript; available in PMC 2012 February 1.…”

Section: Discussionmentioning

confidence: 99%

“…The experiments performed utilized NSAIDs with variable effects on intestinal restitution and variable COX-selectivity, as shown in Table 1 [33][34][35][36]. Drug effects were evaluated over the following ranges of concentrations, as indicated in the text or figure legends: indomethacin (1-100uM); phenylbutazone (1-100uM); NS-398 (1-100uM), SC-560 (10 nM-1uM).…”

Section: Treatment Protocolsmentioning

confidence: 99%

Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution

Freeman

Narváez

McCoy

et al. 2007

Biochemical Pharmacology

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Non-steroidal anti-inflammatory drugs (NSAIDs) contribute to gastrointestinal ulcer formation by inhibiting epithelial cell migration and mucosal restitution; however, the drug-affected signaling pathways are poorly defined. We investigated whether NSAID inhibition of intestinal epithelial migration is associated with depletion of intracellular polyamines, depolarization of membrane potential (E m ) and altered surface expression of K + channels. Epithelial cell migration in response to the wounding of confluent IEC-6 and IEC-Cdx2 monolayers was reduced by indomethacin (100 μM), phenylbutazone (100 μM) and NS-398 (100 μM) but not by SC-560 (1 μM). NSAIDinhibition of intestinal cell migration was not associated with depletion of intracellular polyamines. Treatment of IEC-6 and IEC-Cdx2 cells with indomethacin, phenylbutazone and NS-398 induced significant depolarization of E m , whereas treatment with SC-560 had no effect on E m . The E m of IEC-Cdx2 cells was: −38.5±1.8 mV under control conditions; −35.9±1.6 mV after treatment with SC-560; −18.8±1.2 mV after treatment with indomethacin; and −23.7±1.4 mV after treatment with NS-398. Whereas SC-560 had no significant effects on the total cellular expression of K v 1.4 channel protein, indomethacin and NS-398 decreased not only the total cellular expression of K v 1.4, but also the cell surface expression of both K v 1.4 and K v 1.6 channel subunits in IEC-Cdx2. Both K v 1.4 and K v 1.6 channel proteins were immunoprecipitated by K v 1.4 antibody from IEC-Cdx2 lysates, indicating that these subunits co-assemble to form heteromeric K v channels. These results suggest that NSAID inhibition of epithelial cell migration is independent of polyamine-depletion, and is associated with depolarization of E m and decreased surface expression of heteromeric K v 1 channels.

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“…In this sense, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) includes anti-inflammatory, analgesic and antipyretic effects, via inhibition of cyclooxygenase (COX) enzyme, particularly COX-2, which plays a major role in prostaglandin (PG) synthesis [2,3]. During embryo transfer, manipulation of the reproductive tract produces an inflammatory process which could be induced by the embryo itself, by transfer media acting as foreign material and/or by microorganisms introduced into the uterus during surgery [4].…”

Section: Introductionmentioning

confidence: 99%

Administration of the nonsteroidal anti-inflammatory drug tolfenamic acid at embryo transfer improves maintenance of pregnancy and embryo survival in recipient mice

Schlapp

Goyeneche

Fernandez

et al. 2015

J Assist Reprod Genet

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Purpose To evaluate the effect of the nonsteroidal antiinflammatory drugs tolfenamic acid and flunixin meglumine in pregnancy rate and embryo survival of recipient mice subjected to embryo transfer. Methods A total of 142 recipient females were transferred with 2,931 embryos and treated with a single injection of tolfenamic acid (1 mg/kg; n=54 females with 1,129 embryos), flunixin meglumine (2.5 mg/kg; n=46 females with 942 embryos), or bi-distilled water (10 mL/kg) as control group (n=42 females with 860 embryos). Pregnancy was checked 2 weeks after embryo transfer, delivery was registered on the due date, and litter size was recorded on Day 7 after birth. Results Pregnancy rate of tolfenamic acid treated females was significantly higher than flunixin group (P<0.05) and showed a tendency to be higher when compared to the control group (P=0.06). The number of pups born from transferred embryos in pregnant females was significantly higher for both treatment groups compared to controls (P<0.05). Number of pups from total transferred embryos was higher for both treatment groups (P<0.05) when compared to controls. Conclusion The use of tolfenamic acid at the time of embryo transfer improves both pregnancy rate and number of live pups in recipient mice, with optimal effects observed with flunixin meglumine. We suggest that the use of tolfenamic acid has beneficial effects on the maintenance of pregnancy and embryo survival in recipient mice, which should be taken into account for further studies in other mammalian females.

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In vitro effects of cyclooxygenase inhibitors in whole blood of horses, dogs, and cats

Cited by 179 publications

References 20 publications

Effects of Carprofen and Meloxicam with or without Butorphanol on the Minimum Alveolar Concentration of Sevoflurane in Dogs

Effects of Carprofen and Meloxicam with or without Butorphanol on the Minimum Alveolar Concentration of Sevoflurane in Dogs

Depolarization and decreased surface expression of K+ channels contribute to NSAID-inhibition of intestinal restitution

Administration of the nonsteroidal anti-inflammatory drug tolfenamic acid at embryo transfer improves maintenance of pregnancy and embryo survival in recipient mice

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