Objective: Cardiac remodeling induced by chronic medication of L-thyroxin is manifested by a much more severe cardiac arrhythmias on the occlusion/reperfusion of the coronary artery in rats. A pattern of changes in ion currents in a diseased heart (L-thyroxin induced cardiac remodeling) is possibly provided as a basis of promoting malignant cardiac arrhythmias. An enhanced delayed outward rectifier potassium currents the rapid (IKr) and slow (IKS) component was found in the remodeled heart by L-thyroxin chronic medication. It is interested to investigate the changes in the sodium currents in the L-thyroxin remodeled guinea pig ventricle. Method: The remodeling model in guinea pig was developed by L-thyroxin 4 mg po for 10 days. On d 11, the heart was removed and perfused to isolate ventricular myocytes with medium of Ca2+ free medium containing collagen. The whole cell holding technique was applied. Results: The INa density in the L-thyroxin caused hypertrophied myocytes was reduced significantly at holding potential −30 mV, −53.20 +/−10.78pA/pF against −73.78+/−14.66pA/pF in the normal. (n = 45, p < 0.001). No difference in the steady-state inactivation and recovery kinetics between the remodeled and the normal was found. The recovery constant 37.54+/−3.63 ms in the remodeled vs 36.57+/−2.81 ms in the normal (n = 18, p > 0.05). The accelerated deactivation time constant 3.67+/−0.14 of the remodeled (n = 39) against the normal 4.14+/−0.15 ms (n = 43) (p < 0.05). Conclusion: There is a reduced INa in the L-thyroxin remodeled ventricular myocytes and the deactivation of the current is accelerated. A changed depolarization of the affected myocardium is likely involved in the mechanism of arrhythmogenesis of the remodeled ventricle.
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