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dc.contributor.authorNatnicha Kanlopen_US
dc.contributor.authorKrekwit Shinlapawittayatornen_US
dc.contributor.authorRattapong Sungnoonen_US
dc.contributor.authorPunate Weerateerangkulen_US
dc.contributor.authorSiriporn Chattipakornen_US
dc.contributor.authorNipon Chattipakornen_US
dc.description.abstractPrevious reports demonstrated that cilostazol, a phosphodiesterase 3 inhibitor, affected cellular electrophysiology and reduced episodes of ventricular fibrillation (VF) in patients with Brugada syndrome. However, its effects on VF induction and defibrillation efficacy have never been investigated. We tested the hypothesis that cilostazol increases the VF threshold (VFT) and decreases the upper limit of vulnerability (ULV) and the defibrillation threshold (DFT). A total of 48 pigs were randomly assigned to defibrillation and VF induction studies. The diastolic pacing threshold (DPT), VFT, ULV, DFT, and effective refractory period were determined before and after the infusion of cilostazol at 6 mg/kg, 3 mg/kg, or vehicle. The DPT was significantly increased after administration of 3 and 6 mg/kg cilostazol. The ULV and DFT were significantly decreased after administration of 6 mg/kg cilostazol only. The ULV in the 6 mg/kg group had 12% lower peak voltage and 25% lower total energy, and the DFT had 13% lower peak voltage and 25% lower total energy. The VFT was not altered in any experimental group. This study shows that cilostazol administration significantly increased the DPT, which was associated with significantly reduced DFT and ULV.en_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.subjectPharmacology, Toxicology and Pharmaceuticsen_US
dc.titleCilostazol attenuates ventricular arrhythmia induction and improves defibrillation efficacy in swineen_US
article.title.sourcetitleCanadian Journal of Physiology and Pharmacologyen_US
article.volume88en_US Mai Universityen_US Electrophysiology Uniten_US
Appears in Collections:CMUL: Journal Articles

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