Abstract
The noninfarcted myocardium underwent significant electrophysiological remodelling as part of the healed myocardial infarction remodelling. This study aimed at investigating the effects of nervous growth factor (NGF) on delayed afterdepolarizations (DADs) and triggered activity (TA) of the noninfarcted myocardium in the myocardial infarcted rabbit model. Rabbits with the left anterior descending coronary artery occlusion were prepared and recovered for 8 weeks (HMI group, n = 9). Other rabbits with myocardial infarction were infused NGF to the left stellate ganglion (HMI+NGF group, 400 U/day for 8 weeks, n = 8). Myocytes were isolated from regions of the noninfarcted left ventricular free wall. Action potentials and ion currents were recorded with whole-cell patch clamp. The results showed that more DADs and TA events of HMI+NGF myocytes than that of HMI and Ctrl group. I ti and I Ca-L of NGF+HMI myocytes were increased significantly compared with HMI and Ctrl cells, which contributed to DADs-related triggered arrhythmia. Comparing with HMI and Ctrl myocytes, significant prolongations of APD 50 and APD 90 in HMI+NGF myocytes were found. The results indicated the electrophysiological change of HMI myocytes with NGF infusion. It suggested that more events of DADs and TA in HMI myocytes with NGF treatment. The underlying mechanism may be involved in the increase of I ti and I Ca-L .
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