Publication:
Hyperbaric oxygen therapy prevents subarachnoid hemorrhage-induced apoptosis and impaired contractility of the rabbit bladder

dc.contributor.coauthorTinay, İlker
dc.contributor.coauthorÇelik, Özgür
dc.contributor.coauthorŞekerci, Çağrı, Akın
dc.contributor.coauthorÇadırcı, Selin
dc.contributor.coauthorÇevik, Özge
dc.contributor.coauthorOroglu, Bengusu
dc.contributor.coauthorŞener, Göksel
dc.contributor.kuauthorTarcan, Tufan
dc.contributor.kuprofileOther
dc.contributor.yokid173289
dc.date.accessioned2024-11-09T23:38:13Z
dc.date.issued2020
dc.description.abstractAim: To explore the effects of experimental subarachnoid hemorrhage (SAH) on rabbit urinary bladder and to assess the potential protective effects of hyperbaric oxygen therapy (HBOT). Methods: A total of 15 male New Zealand white rabbits were divided randomly to one of three groups: group I was spared as the control group (n = 5), group II was exposed to SAH, received no treatment, and acted as the SAH group (n = 5) and group III was exposed to SAH and received five sessions of HBOT (started 12 hours after SAH induction and was given twice daily for the first 2 days and once on the third day) and acted as the treatment group (n = 5). At 72 hours after the SAH induction, bladders from all animals were removed for in vitro organ bath experiments and biochemical analyses. Results: Isometric tension studies revealed that compared to group I, the contractile responses of the strips to carbachol in group II were significantly decreased whereas HBOT restored the contractile responses (P < .05). Caspase-3 and nitric oxide synthase (NOS) activities of bladder tissues were significantly increased in group II when compared with group I, whereas caspase-3 and NOS activities were significantly decreased in the tissues of group III (P < .01). Conclusions: Subarachnoid hemorrhage stimulates apoptosis of the rabbit bladder and impairs the contractile response of the rabbit bladder to carbachol. HBOT creates a protective effect in rabbit bladder tissues and restores SAH-induced changes.
dc.description.indexedbyWoS
dc.description.indexedbyScopus
dc.description.indexedbyPubMed
dc.description.issue5
dc.description.openaccessNO
dc.description.publisherscopeInternational
dc.description.volume39
dc.identifier.doi10.1002/nau.24418
dc.identifier.eissn1520-6777
dc.identifier.issn0733-2467
dc.identifier.quartileQ2
dc.identifier.scopus2-s2.0-85085891785
dc.identifier.urihttp://dx.doi.org/10.1002/nau.24418
dc.identifier.urihttps://hdl.handle.net/20.500.14288/12928
dc.identifier.wos536779200001
dc.keywordsApoptosis
dc.keywordsHyperbaric oxygene therapy
dc.keywordsSubarachnoid heamorrhage
dc.keywordsUrinary bladder cerebral-ischemia
dc.keywordsDysfunction
dc.keywordsDamage
dc.keywordsTime
dc.languageEnglish
dc.publisherWiley
dc.sourceNeurourology and Urodynamics
dc.subjectUrology
dc.subjectNephrology
dc.titleHyperbaric oxygen therapy prevents subarachnoid hemorrhage-induced apoptosis and impaired contractility of the rabbit bladder
dc.typeJournal Article
dspace.entity.typePublication
local.contributor.authorid0000-0002-3387-3524
local.contributor.kuauthorTarcan, Tufan
local.publication.orgunit1SCHOOL OF MEDICINE
local.publication.orgunit2School of Medicine

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