| Autor: |
Brunner, Michael, Kodirov, Sodikdjon A., Mitchell, Gary F., Buckett, Peter D., Shibata, Katsushi, Folco, Eduardo J., Baker, Linda, Salama, Guy, Chan, Danny P., Jun Zhou, Koren, Gideon |
| Předmět: |
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| Zdroj: |
American Journal of Physiology: Heart & Circulatory Physiology; Jul2003, Vol. 285 Issue 1, pH194, 10p, 2 Color Photographs, 5 Black and White Photographs, 1 Chart, 24 Graphs |
| Abstrakt: |
Mutations in cardiac voltage-gated K[sup +] channels cause long QT syndrome (LQTS) and sudden death. We created a transgenic mouse with a long QT phenotype (Kv1DN) by overexpression of a truncated K[sup +] channel in the heart and investigated whether the dominant negative effect of the transgene would be overcome by the direct injection of adenoviral vectors expressing wild-type Kv1.5 (AV-Kv1.5) into the myocardium. End points at 3-10 days included electrophysiology in isolated cardiomyocytes, surface ECG, programmed stimulation of the right ventricle, and in vivo optical mapping of action potentials and repolarization gradients in Langendorff-perfused hearts. Overexpression of Kv1.5 reconstituted a 4-aminopyridine-sensitive outward K[sup +] current, shortened the action potential duration, eliminated early after depolarizations, shortened the QT interval, decreased dispersion of repolarization, and increased the heart rate. Each of these changes is consistent with a physiologically significant primary effect of adenoviral expression of Kv1.5 on ventricular repolarization of Kv1DN mice. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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