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dc.contributor.authorChang, Po-Chengen_US
dc.contributor.authorLu, Yu-Yingen_US
dc.contributor.authorLee, Hui-Lingen_US
dc.contributor.authorLin, Shien-Fongen_US
dc.contributor.authorChu, Yenen_US
dc.contributor.authorWen, Ming-Shienen_US
dc.contributor.authorChou, Chung-Chuanen_US
dc.date.accessioned2019-04-02T06:00:34Z-
dc.date.available2019-04-02T06:00:34Z-
dc.date.issued2018-08-01en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://dx.doi.org/10.1097/FJC.0000000000000598en_US
dc.identifier.urihttp://hdl.handle.net/11536/148253-
dc.description.abstractCalcium homeostasis plays an important role in development of early afterdepolarizations (EADs) and torsade de pointes (TdP). The role of sodium-calcium exchanger (NCX) inhibition in genesis of secondary Ca2+ rise and EAD-TdP is still debated. Dual voltage and intracellular Ca2+ optical mapping were conducted in 6 control and 9 failing rabbit hearts. After baseline electrophysiological and optical mapping studies, E4031 was given to simulate long QT syndrome. ORM-10103 was then administrated to examine the electrophysiological effects on EAD-TdP development. E4031 enhanced secondary Ca2+ rise, EADs development, and TdP inducibility in both control and failing hearts. The results showed that ORM-10103 reduced premature ventricular beats but was unable to suppress the inducibility of TdP or EADs. The electrophysiological effects of ORM-10103 included prolongation of action potential duration (APD) and increased APD heterogeneity in failing hearts. ORM-10103 had a neutral effect on the amplitude of secondary Ca-1 rise in control and heart failure groups. In this model, most EADs generated from long-short APD junction area. In conclusion, highly selective NCX inhibition with ORM-10103 reduced premature ventricular beat burden but was unable to suppress secondary Ca2+ rise, EADs development, or inducibility of TdP. The possible electrophysiological mechanisms include APD prolongation and increased APD heterogeneity.en_US
dc.language.isoen_USen_US
dc.subjectheart failureen_US
dc.subjectsodium-calcium exchangersen_US
dc.subjecttorsade de pointesen_US
dc.subjectearly afterdepolarizationsen_US
dc.titleParadoxical Effects of Sodium-Calcium Exchanger Inhibition on Torsade de Pointes and Early Afterdepolarization in a Heart Failure Rabbit Modelen_US
dc.typeArticleen_US
dc.identifier.doi10.1097/FJC.0000000000000598en_US
dc.identifier.journalJOURNAL OF CARDIOVASCULAR PHARMACOLOGYen_US
dc.citation.volume72en_US
dc.citation.spage97en_US
dc.citation.epage105en_US
dc.contributor.department分子醫學與生物工程研究所zh_TW
dc.contributor.departmentInstitute of Molecular Medicine and Bioengineeringen_US
dc.identifier.wosnumberWOS:000446477900003en_US
dc.citation.woscount1en_US
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