The changes of potassium currents in rabbit ventricle with healed myocardial infarction.
- Author:
Nian LIU
1
;
Huiyan NIU
;
Yang LI
;
Cuntai ZHANG
;
Qiang ZHOU
;
Yanfei RUAN
;
Jun PU
;
Zaiying LU
Author Information
1. Department of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
- Publication Type:Journal Article
- MeSH:
Action Potentials;
Animals;
Arrhythmias, Cardiac;
etiology;
Female;
Heart Ventricles;
metabolism;
Male;
Myocardial Infarction;
complications;
metabolism;
pathology;
Myocytes, Cardiac;
cytology;
Patch-Clamp Techniques;
Potassium Channels;
metabolism;
Rabbits
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2004;24(2):128-131
- CountryChina
- Language:English
-
Abstract:
To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), the changes of action potential duration (APD), transient outward potassium current (Ito), delayed rectifier potassium current (IK) and inward rectifier potassium current (IK1) of left ventricular myocytes 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, Ito, IK, and IK1 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 Ito, I(K, tail), and IK1 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 Ito, I(K, tail) and IK1 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.
