Alteration of ion channel currents in ventricular myocytes of the rabbit 24 hours after acute myocardial infarction

Chao DING; Zhenshan HE; Junyu CUI; Xiaoyun LIU; Li YANG

ABSTRACT

BACKGROUND:

After acute myocardial infarction(AMI),there is still surviving myocardium in and around the infarcted area,which plays an important role in the occurrence of arrhythmia.

OBJECTIVE:

To study the alterations of the activities of Na+ channel current(INa),L-calcium current(ICa-L),transient outward K+ current(Ito) and inward rectifying K+ current(IK1) in the cardiomyocytes in the infarcted area after AMI.

DESIGN:

A randomized controlled study.

SETTING:

Department of Cardiology,Bethune International Peace Hospital.

PARTICIPANTS:

The experiment was finished in the Central Laboratory of the Department of Cardiology,Bethune International Peace Hospital from January to June 2003.Twenty New Zealand pure big-ear rabbits were randomly divided into AMI group(n=10) and control group(n=10).

INTERVENTIONS:

Rabbit AMI models were established by ligation of the left anterior descending coronary artery.The ventricular myocytes were separated with the method of enzymatic dissociation technique,and the changes of the ion currents were recorded with the whole cell patch-clamp techniques. MAIN OUTCOME

MEASURES:

The changes of INa,ICa-L,Ito and IK1 in the cardiomyocytes taken from the infarcted area of epicardium 24 hours after AMI in both the AMI and control groups.

RESULTS:

Twenty-four hours after AMI,the peak current densities of INa,ICa-L and IK1 in the AMI group [(28.48± 3.53) pA/pF,n=16;(3.91± 0.95) pA/pF,n=12;(26.93 ± 3.48) pA/pF,n=16]were all significantly reduced as compared with those in the control group [(45.50± 5.33) pA/pF,n=12;(5.58± 1.53) pA/pF,n=10;(34.12± 4.21) pA/pF,n=10] (t=3.026,P< 0.01;t=2.985,P< 0.01;t=2.706,P< 0.05).There was no significant difference in the Ito density between the AMI group and control group (P >0.05).

CONCLUSION:

The reduce of INa,ICa-L and IK1 caused by AMI can result in the decrease of myocardial conduction velocity,the shortening of action potential-time,abnormal repolarization,which is possibly the ionic mechanism for the reentrant ventricular arrhythmia after AMI.