dc.creatorVargas, Claudio Gonzalez
dc.creatorMiranda, Hugo F.
dc.creatorSierralta, Fernando
dc.creatorNoriega, Viviana
dc.creatorPrieto, Juan Carlos
dc.date.accessioned2019-10-15T12:25:32Z
dc.date.available2019-10-15T12:25:32Z
dc.date.created2019-10-15T12:25:32Z
dc.date.issued2019
dc.identifierDrug Development Research, Volumen 80, Issue 4, 2019, Pages 471-474
dc.identifier10982299
dc.identifier02724391
dc.identifier10.1002/ddr.21519
dc.identifierhttps://repositorio.uchile.cl/handle/2250/171715
dc.description.abstractNonsteroidal 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
dc.languageen
dc.publisherWiley-Liss Inc.
dc.rightshttp://creativecommons.org/licenses/by-nc-nd/3.0/cl/
dc.rightsAttribution-NonCommercial-NoDerivs 3.0 Chile
dc.sourceDrug Development Research
dc.subjectclomipramine
dc.subjectmouse visceral pain
dc.subjectNSAIDs
dc.subjectpharmacological interaction
dc.subjectrisperidone
dc.subjecttonic pain
dc.titlePharmacological interaction between NSAIDS with clomipramine and risperidone in mice visceral pain
dc.typeArtículo de revista


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