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dc.contributor.author Boros, Krisztina
dc.contributor.author Jancsó, Gábor
dc.contributor.author Dux, Mária
dc.contributor.author Fekécs, Zoltán
dc.contributor.author Bencsik, Péter
dc.contributor.author Oszlács, Orsolya
dc.contributor.author Jancsó Gáborné Katona, Márta
dc.contributor.author Ferdinandy, Péter
dc.contributor.author Nógrádi, Antal
dc.contributor.author Sántha, Péter
dc.date.accessioned 2018-09-04T08:03:16Z
dc.date.available 2018-09-04T08:03:16Z
dc.date.issued 2016
dc.identifier 84976328462
dc.identifier.citation pagination=1009-1020; journalVolume=389; journalIssueNumber=9; journalTitle=NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/6225
dc.identifier.uri doi:10.1007/s00210-016-1267-x
dc.description.abstract Besides their deleterious action on cardiac muscle, anthracycline-type cytostatic agents exert significant neurotoxic effects on primary sensory neurons. Since cardiac sensory nerves confer protective effects on heart muscle and share common traits with cutaneous chemosensitive nerves, this study examined the effects of cardiotoxic doses of adriamycin on the function and morphology of epidermal nerves. Sensory neurogenic vasodilatation, plasma extravasation, and the neural CGRP release evoked by TRPV1 and TRPA1 agonists in vitro were examined by using laser Doppler flowmetry, the Evans blue technique, and ELISA, respectively. Carrageenan-induced hyperalgesia was assessed with the Hargreaves method. Immunohistochemistry was utilized to study cutaneous innervation. Adriamycin treatment resulted in profound reductions in the cutaneous neurogenic sensory vasodilatation and plasma extravasation evoked by the TRPV1 and TRPA1 agonists capsaicin and mustard oil, respectively. The in vitro capsaicin-, but not high potassium-evoked neural release of the major sensory neuropeptide, CGRP, was markedly attenuated after adriamycin treatment. Carrageenan-induced inflammatory hyperalgesia was largely abolished following the administration of adriamycin. Immunohistochemistry revealed a substantial loss of epidermal TRPV1-expressing nociceptive nerves and a marked thinning of the epidermis. These findings indicate impairments in the functions of TRPV1 and TRPA1 receptors expressed on cutaneous chemosensitive nociceptive nerves and the loss of epidermal axons following the administration of cardiotoxic doses of adriamycin. Monitoring of the cutaneous nociceptor function in the course of adriamycin therapy may well be of predictive value for early detection of the deterioration of cardiac nerves which confer protection against the deleterious effects of the drug.
dc.relation.ispartof urn:issn:0028-1298
dc.title Multiple impairments of cutaneous nociceptor function induced by cardiotoxic doses of Adriamycin in the rat
dc.type Journal Article
dc.date.updated 2018-08-28T18:35:13Z
dc.language.rfc3066 en
dc.identifier.mtmt 3088769
dc.identifier.wos 000381404000007
dc.identifier.pubmed 27342418
dc.contributor.department SE/AOK/I/Farmakológiai és Farmakoterápiás Intézet
dc.contributor.institution Semmelweis Egyetem


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