抄録
Cardiac hypertrophy is an adaptive response to chronic cardiac overload, and causes an abnormal electrical activity leading to arrhythmia. It is important to understand the electrophysiological mechanisms underlying the development of this condition. Therefore we analyzed the electrocardiogram (ECG) in hypertrophic heart of mice persistently pressure-overloaded by transverse aortic constriction (TAC). In pre-operated or sham-operated (SO) mice, the first upstroke in QRS-complex (designed to as "a") is followed by a fast second upstroke ("b") and sometimes a slower downstroke ("c"). In TAC mice, "b" is often followed by another slow upstroke ("b'") before "c", and a prolongation of Qc interval was revealed. These results suggest that ECG is sensitive enough to confirm development of cardiac hypertrophy in TAC mice. In addition, the whole-cell patch clamp recordings showed a prolongation of the action potential duration (APD) and a basal activation of chloride (Cl−) current in single myocytes freshly isolated from left ventricle of TAC mice. The Cl− current may reflect a persistent activation of volume-regulated Cl− current (ICl,vol) in isotonic condition, because of the time-dependent inactivation at higher positive potentials, the outwardly rectifier current-voltage relationships and the inhibitory effect of 4,4'-Diisothiocyanatostilbene-2,2'-disulphonic acid. The basal activation of ICl,vol may be responsible for prolongation of APD and Qc interval in TAC mice. [J Physiol Sci. 2006;56 Suppl:S129]
