Pharmacological interaction between NSAIDS with clomipramine and risperidone in mice visceral pain
Author
dc.contributor.author
Vargas, Claudio Gonzalez
Author
dc.contributor.author
Miranda, Hugo F.
Author
dc.contributor.author
Sierralta, Fernando
Author
dc.contributor.author
Noriega, Viviana
Author
dc.contributor.author
Prieto, Juan Carlos
Admission date
dc.date.accessioned
2019-10-15T12:25:32Z
Available date
dc.date.available
2019-10-15T12:25:32Z
Publication date
dc.date.issued
2019
Cita de ítem
dc.identifier.citation
Drug Development Research, Volumen 80, Issue 4, 2019, Pages 471-474
Identifier
dc.identifier.issn
10982299
Identifier
dc.identifier.issn
02724391
Identifier
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10.1002/ddr.21519
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/171715
Abstract
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Nonsteroidal anti-inflammatory drugs (NSAIDs) possess as primary action mechanism the inhibition of cyclooxygenases (COX-1, COX-2, and COX-3), thus producing a decreasing prostaglandin synthesis. This study was designed to evaluate whether the antinociception induced by NSAIDs could be modulated by clomipramine or risperidone using a chemical model of inflammatory acute visceral pain, the abdominal acetic acid induced a writhing test in mice. Dose–response curves, intraperitoneal, or intrathecal for the antinociceptive activity displayed by ketoprofen, piroxicam, nimesulide, parecoxib, and paracetamol were analyzed in order to obtain the ED50 of each drug. Pretreatment of mice with either clomipramine or risperidone, increased antinociceptive potency of ketoprofen, piroxicam, nimesulide, parecoxib, and paracetamol, expressed by a decrease in the values of antinociceptive ED50. The results that were obtained are in line with those where the inhibition of CO