首页|The Changes of Potassium Currents in Rabbit Ventricle with Healed Myocardial Infarction
The Changes of Potassium Currents in Rabbit Ventricle with Healed Myocardial Infarction
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To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), the changes of action potential duration (APD), transient outward potassium current (I_(to)), delayed rectifier potassium current (I_K) and inward rectifier potassium current (I_(K1)) of left ventricular myo-cytes in non-infarcted zone of HMI were investigated. Rabbits were randomly assigned into two groups: HMI group, in which animals were subjected to thoracotomy and ligation of the circumflex coronary and sham-operated group, in which rabbits underwent thoracotomy but no conorary ligation. 3 months after the operation, the whole myocyte patch clamp technique was used to record APD, I_(to), I_K, and I_(K1) of ventricular myocytes in non-infarcted zone. Our results showed that the membrane capacitance was larger in HMI group than in sham-operated group. Action potential duration was significantly lengthened in HMI group and early afterdepolarization (EAD) appeared in HMI group. The densities of I_(to), I_(K, tail) , and I_(K1) were reduced significantly in HMI group, from 6. 72 +- 0. 42 pA/pF, 1. 54 +- 0. 13 pA/pF and 25. 6 +- 2. 6 pA/pF in sham-operated group to 4. 03 +- 0. 33 pA/pF, 1. 14 +- 0. 11 pA/pF and 17. 6 +- 2. 3 pA/pF, respectively. It is concluded that the reduced densities of I_(to), I_(K, tail) and I_(K1) in ventricular myocytes of non-infarcted zone in HMI were responsible for the prolongation of APD and the presentation of EAD which played important roles in the development of malignant arrhythmia in HMI.
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