Model-Dependent Effects of the Gap Junction Conduction–Enhancing Antiarrhythmic Peptide Rotigaptide (ZP123) on Experimental Atrial Fibrillation in Dogs | Zendy

Akiko Shiroshita-Takeshita | Zendy; Masao Sakabe | Zendy; Ketil Haugan | Zendy; James K. Hennan | Zendy; Stanley Nattel | Zendy

Open Access

Model-Dependent Effects of the Gap Junction Conduction–Enhancing Antiarrhythmic Peptide Rotigaptide (ZP123) on Experimental Atrial Fibrillation in Dogs

Author(s) -

Akiko Shiroshita-Takeshita,

Masao Sakabe,

Ketil Haugan,

James K. Hennan,

Stanley Nattel

Publication year - 2007

Publication title -

circulation

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 7.795

H-Index - 607

eISSN - 1524-4539

pISSN - 0009-7322

DOI - 10.1161/circulationaha.106.665547

Subject(s) - medicine , atrial fibrillation , cardiology , gap junction , anti arrhythmia agents , electrical conduction system of the heart , fibrillation , antiarrhythmic agent , electrocardiography , heart disease , intracellular , biology , microbiology and biotechnology

Abnormal intercellular communication caused by connexin dysfunction may be involved in atrial fibrillation (AF). The present study assessed the effect of the gap junctional conduction-enhancing peptide rotigaptide on AF maintenance in substrates that result from congestive heart failure induced by 2-week ventricular tachypacing (240 bpm), atrial tachypacing (ATP; 400 bpm for 3 to 6 weeks), and isolated atrial myocardial ischemia.

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