Second Pathways in the Pathophysiology of Ischemic Priapism and Treatment Alternatives

dc.contributor.authorKarakeci, Ahmet
dc.contributor.authorFirdolas, Fatih
dc.contributor.authorOzan, Tunc
dc.contributor.authorUnus, Ihsan
dc.contributor.authorOgras, Mehmet Sezai
dc.contributor.authorOrhan, Irfan
dc.date.accessioned2026-08-12T17:32:01Z
dc.date.issued2013
dc.departmentFırat Üniversitesi
dc.description.abstractOBJECTIVE To evaluate the early therapeutic alternatives such as bosentan, an endothelin receptor blocker, theophylline, an adenosin receptor blocker, and a nonselective phosphodiesterase enzyme inhibitor, zinc protoporphyrin (ZnPP), a heme oxygenase 1 inhibitor, for the therapy of ischemic priapism in the rat models. METHODS Twenty-four Sprague-Dawley rats were randomly divided into 4 equal groups: control group, ZnPP group, bosentan group, and theophylline group. Erection was provided by vacuum constriction method and maintained for 4 hours for achieving the priapism in all groups. The rats in the control group were administered 1 mL/kg saline intraperitoneally (ip). The rats in group 2 were administered 25 mg/kg ZnPP ip. The rats in group 3 were administered 0.25 mg/kg bosentan ip. The rats in group 4 were administered 100 mg/kg theophylline ip. Six rats from each group were decapitated after 6 hours of drug administration. Then endothelin 1, adenosine deaminase, heme oxygenase 1 enzymatic activity, and apoptosis index in the cavernous tissues were estimated. RESULTS Cavernous tissue endothelin 1, adenosine deaminase, heme oxygenase 1 enzymatic activity levels, and apoptosis index were significantly decreased in bosentan, theophylline, and ZnPP-treated rats compared with the controls. CONCLUSION Inhibition of priapism induced apoptosis with bosentan, theophylline, and ZnPP seems promising on preserving erectile function. UROLOGY 82: 625-629, 2013. (C) 2013 Elsevier Inc.
dc.identifier.doi10.1016/j.urology.2013.06.029
dc.identifier.endpage629
dc.identifier.issn0090-4295
dc.identifier.issn1527-9995
dc.identifier.issue3
dc.identifier.orcid0000-0002-7417-8413
dc.identifier.orcid0000-0003-2097-9853
dc.identifier.pmid23987157
dc.identifier.scopus2-s2.0-84883234656
dc.identifier.scopusqualityQ2
dc.identifier.startpage625
dc.identifier.urihttps://doi.org/10.1016/j.urology.2013.06.029
dc.identifier.urihttps://hdl.handle.net/11508/56465
dc.identifier.volume82
dc.identifier.wosWOS:000323790800043
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Science Inc
dc.relation.ispartofUrology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260511
dc.subjectAdenylate-Cyclase
dc.subjectHeme Oxygenase-1
dc.subjectAdenosine
dc.subjectInhibition
dc.subjectMonoxide
dc.subjectTissues
dc.titleSecond Pathways in the Pathophysiology of Ischemic Priapism and Treatment Alternatives
dc.typeArticle

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