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Changes of potassium currents in rabbit ventricle with healed myocardial infarction
Authors:LIU Nian  NIU Hui-yan  LI Yang  ZHANG Cun-tai  ZHOU Qiang  RUAN Yan-fei  PU Jun  LU Zai-ying
Affiliation:Department of Cardiology, Tongji Hospital, Tongji Medical College, Hua Zhong University of Science and Technology, Wuhan 430030, China
Abstract:AIM: To elucidate the mechanism of arrhythmia in healed myocardial infarction (HMI), and to investigate 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 noninfarcted zone of HMI. METHODS: 12 rabbits were randomly assigned in two groups: HMI group (thoracotomy and ligation of the circumflex coronary); sham-operated group (thoracotomy but no conorary ligation). 3 months after operation, whole cell patch clamp technique was used to record APD, Ito, IK and IK1 of ventricular myocytes in non-infarcted zone. RESULTS: Membrane capacitance was larger in HMI group than that in sham-operated group. Action potential duration was lengthened significantly in HMI group and early after depolarization (EAD) appeared in HMI group. The densities of Ito, IK,tail and IK1 were reduced significantly in HMI group (P<0.01), 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. CONCLUSION: The reduced densities of Ito, IK,tail and IK1 in ventricular myocytes of non-infarcted zone in HMI are responsible for the prolongation of APD and the presentation of EAD, which play important roles in the malignant arrhythmia of HMI.
Keywords:Myocardial infarction  Potassium channels  Patch clamp techniques  
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