Electrophysiology of papillary muscle in SAH: changes and N-acetylcysteine protection

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dc.contributor.authorAyaz, Murat
dc.contributor.authorGuney, Onder
dc.contributor.authorErdi, Fatih
dc.contributor.authorKucukbagriacik, Yusuf
dc.date.accessioned2020-03-26T17:38:32Z
dc.date.available2020-03-26T17:38:32Z
dc.date.issued2009
dc.departmentSelçuk Üniversitesien_US
dc.description.abstractAlthough subarachnoid hemorrhage (SAH) serves as a good model to study heart-brain interactions, neither the changes on the single ventricular action potential (SVAP) and contraction nor the effects of possible cardioprotective agents have been investigated. A total of 18 male rabbits were used for the three experimental groups. SAH was induced by replacing the cerebrospinal fluid (CSF) with fresh autologous blood at the ratio of 1 mL to the 1-kg body mass (N = 6). In the control (CON; N = 6) group, the CSF was replaced with serum physiologic at the same ratio. The treated SAH group (SAH+NAC) received daily intraperitoneal N-acetylcysteine (NAC; 150 mg/kg for 3 days) starting from just before SAH was induced by CSF replacement. On the fourth day, animals were examined for the single action potential and contraction recordings from the left ventricular papillary muscle. At the end of 3 days, the overshoot decreased together with increased time to reach the peak potential. Additionally, the resting membrane potential was depressed and repolarization was slowed during SVAPs. On the other hand, peak tension depressed and time to peak increased. NAC treatment, which protects infarction in the brain, prevented these pathological changes in the cardiac muscle. SAH-induced cardiac changes can be attributed to adenosine triphosphate depletion through mitochondrial dysfunction. Pretreatment of NAC to SAH on the other hand had a positive effect on these cardiac changes. But the exact mechanism by which NAC treatment protects the cardiac muscle needs further investigation.en_US
dc.identifier.doi10.1007/s10840-009-9400-0en_US
dc.identifier.endpage100en_US
dc.identifier.issn1383-875Xen_US
dc.identifier.issn1572-8595en_US
dc.identifier.issue2en_US
dc.identifier.pmid19399602en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage95en_US
dc.identifier.urihttps://dx.doi.org/10.1007/s10840-009-9400-0
dc.identifier.urihttps://hdl.handle.net/20.500.12395/23508
dc.identifier.volume26en_US
dc.identifier.wosWOS:000272174700002en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSPRINGERen_US
dc.relation.ispartofJOURNAL OF INTERVENTIONAL CARDIAC ELECTROPHYSIOLOGYen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectSubarachnoid hemorrhageen_US
dc.subjectPapillary muscleen_US
dc.subjectElectrophysiologyen_US
dc.subjectN-acetylcysteineen_US
dc.titleElectrophysiology of papillary muscle in SAH: changes and N-acetylcysteine protectionen_US
dc.typeArticleen_US

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