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Role of sarcoplasmic reticulum calcium in development of secondary calcium rise and early afterdepolarizations in long QT syndrome rabbit model.
Chang, Po-Cheng; Wo, Hung-Ta; Lee, Hui-Ling; Lin, Shien-Fong; Wen, Ming-Shien; Chu, Yen; Yeh, San-Jou; Chou, Chung-Chuan.
Affiliation
  • Chang PC; Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Linko, Taoyuan, Taiwan; Chang Gung University College of Medicine, Taoyuan, Taiwan.
  • Wo HT; Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Linko, Taoyuan, Taiwan.
  • Lee HL; Department of Anesthesia, Chang Gung Memorial Hospital, Taipei, Taiwan.
  • Lin SF; Institute of Biomedical Engineering, National Chiao Tung University, Hsin Chu, Taiwan.
  • Wen MS; Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Linko, Taoyuan, Taiwan; Chang Gung University College of Medicine, Taoyuan, Taiwan.
  • Chu Y; Chang Gung University College of Medicine, Taoyuan, Taiwan; Division of Thoracic Surgery, Chang Gung Memorial Hospital, Linko, Taoyuan, Taiwan; Institute of Biomedical Engineering, National Chiao Tung University, Hsin Chu, Taiwan.
  • Yeh SJ; Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Linko, Taoyuan, Taiwan; Chang Gung University College of Medicine, Taoyuan, Taiwan.
  • Chou CC; Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Linko, Taoyuan, Taiwan; Chang Gung University College of Medicine, Taoyuan, Taiwan.
PLoS One ; 10(4): e0123868, 2015.
Article in En | MEDLINE | ID: mdl-25875599
BACKGROUND: L-type calcium current reactivation plays an important role in development of early afterdepolarizations (EADs) and torsades de pointes (TdP). Secondary intracellular calcium (Cai) rise is associated with initiation of EADs. OBJECTIVE: To test whether inhibition of sarcoplasmic reticulum (SR) Ca2+ cycling suppresses secondary Cai rise and genesis of EADs. METHODS: Langendorff perfusion and dual voltage and Cai optical mapping were conducted in 10 rabbit hearts. Atrioventricular block (AVB) was created by radiofrequency ablation. After baseline studies, E4031, SR Ca2+ cycling inhibitors (ryanodine plus thapsigargin) and nifedipine were then administrated subsequently, and the protocols were repeated. RESULTS: At baseline, there was no spontaneous or pacing-induced TdP. After E4031 administration, action potential duration (APD) was significantly prolonged and the amplitude of secondary Cai rise was enhanced, and 7 (70%) rabbits developed spontaneous or pacing-induced TdP. In the presence of ryanodine plus thapsigargin, TdP inducibility was significantly reduced (2 hearts, 20%, p = 0.03). Although APD was significantly prolonged (from 298 ± 30 ms to 457 ± 75 ms at pacing cycle length of 1000 m, p = 0.007) by ryanodine plus thapsigargin, the secondary Cai rise was suppressed (from 8.8 ± 2.6% to 1.2 ± 0.9%, p = 0.02). Nifedipine inhibited TdP inducibility in all rabbit hearts. CONCLUSION: In this AVB and long QT rabbit model, inhibition of SR Ca2+ cycyling reduces the inducibility of TdP. The mechanism might be suppression of secondary Cai rise and genesis of EADs.
Subject(s)

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Sarcoplasmic Reticulum / Long QT Syndrome / Action Potentials / Calcium Type of study: Prognostic_studies Limits: Animals Language: En Journal: PLoS One Journal subject: CIENCIA / MEDICINA Year: 2015 Document type: Article Affiliation country: Country of publication:

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Sarcoplasmic Reticulum / Long QT Syndrome / Action Potentials / Calcium Type of study: Prognostic_studies Limits: Animals Language: En Journal: PLoS One Journal subject: CIENCIA / MEDICINA Year: 2015 Document type: Article Affiliation country: Country of publication: