| Objective: To investigate the electrophysiological mechanism of QT prolongation in mice with alcoholic cardiomyopathy(ACM) induced by chonic alcohol intake. Methods: A total of 40 C57BL/6 mice were randomly divided into 2 groups: Alcoholic group, n=25, the ACM mouse model was established by long term alcohol drinking with water and intragastric alcohol administration, 12 mice died during feeding period and anesthesia process, and 13 mice were enrolled into final study. Control group, n=15, the mice were fed by normal diet, 3 died during anesthesia and 12 were enrolled for study. After 5 months deeding, the pathological changes of ACM were examined by electric microscope, QT interval was measured by ECG, the electrophysiology of cell action potential duration and the functions of ion channels were studied by whole cell patch-clamp techniques. Results: Alcohol group showed decreased left ventricle ejection fraction(LVEF) than in control group(39.06 ± 1.511) % vs(61.18 ± 2.56) %, prolonged QT interval(106.43 ± 5.91) ms vs(85.64 ± 6.35) ms, P<0.05, and prolonged action potential duration APD90(37.62 ± 3.53) ms vs(25.77 ± 3.41) ms. The voltage-dependent inactivation of L-type Ca2+ channels was delayed and window current increased. Conclusion: Long term alcohol drinking may cause delayed inactivation of myocardium Ca2+ channel, prolong the action potential duration, which is one of the mechanisms for prolonged QT interval of ACM in mice. |
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