T.-M. Feng’s scientific contributions

Aim: To investigate the effects of matrine on the rapid component of delayed rectifier potassium current (IKr) in ischemic or/and acidic ventricular myocytes. Methods: In isolated ventricular myocytes of guinea pig, the effects of matrine on IKr were observed by using the whole cell patch clamp technique at pH =7.4 and pH =6.5. After ligation of left anterior descending coronary artery and giving matrine by oral administration for one month, whole cell patch clamp technique was used to record IKr in isolated rabbit ventricular myocytes. Results: In ventricular myocytes of guinea pig, matrine (50 μmol·L-1) inhibited IKr significantly in the nomal extracellular fluid (pH =7.4). At test potential of +60 mV, the IKr density was decreased from(12.15 ± 0.70) pA/pF to (9.22 ± 0.65) pA/pF (n = 8, P < 0.05). Matrine could also inhibit IKr significantly in the acidifying extracellular fluid. At test potential of + 60 mV, the IKr density was decreased from (7.05 ± 0.41) pA/pF to (5.76 ± 0.28) pA/pF (n = 8, P < 0.05). At test potential of + 60 mV, The IKr density of myocardial cells from one month post-infarcted rabbit hearts (1.17 ± 0.12) pA/pF depressed obviously compared with that of nomal group (1.70 ± 0.11) pA/pF (n = 12, P < 0.05). After oral administration of matrine (8 mg·kg -1·d-1) to the post-infarcted rabbits for one-month period, the IKr density of matrine group (0.86 ± 0. 25) pA/pF reduced markedly compared with that of MI group (n = 12, P < 0.05). Conclusions: The inhibitory effect of matrine on IKr may contribute to its antiarrhythmic action. Matrine may be useful in treatment of ischemic arrhythmias as it is effective in acidic ventricular myocytes or post-infarcted hearts.

Aim: To approach the antiarrhythmic effects of adenosine and the synergistic antiarrhythmic effects of combination of adenosine and dipyridamole. Methods: Different drugs were injected into rats through vena caudalis. The electrocardiogram (ECG) was recorded and analyzed by using BL-420E system. Results: Adenosine significantly prolonged the R-R interval in a dose-dependent manner and the effects were enhanced by combination with dipyridamole. Adenosine terminated ventricular arrhythmia induced by adrenalin and BaCl2 in rats and the antiarrhythmic effects were prolonged by combination with dipyridamole. Conclusion: Adenosine antagonized the ventricular arrhythmias induced by adrenalin and BaCl2 in rats and the antagonism was enhanced by combination with dipyridamole.

Objective: To observe the effect of quinidine on sodium current of ventricular myocytes from post-ischaemic rats so as to explore the proarrhythmic mechanisms of quinidine. Methods: The left anterior descending (LAD) coronary artery was ligated to establish the ischemia head model in Wistar rats. Quinidine (10 mg·kg-1·d-1) was administered to rats with coronary occlusion for 3 months. Whole-cell patch clamp techniques were used to record sodium current (INa). Results: The morbidity rate of post-ischemic rats was increased by chronic application of quinidine. At the test potential of - 30 mV, the sodium current amplitude of ventricular myocytes from quinidine-treated group was significantly decreased to - (1284 ± 129) pA from - (1985 ± 204) pA in ischemic group (t = 3.015,P < 0.01). Conclusions: Sodium current was sensitive to quinidine even in post-ischemic heart. The different effects of quinidine on different currents in post-ischemic heart resulted in imbalance of ionic currents of ischemic heart. That may be the ionic mechanism of proarrhythmic effect of chronic application of quinidine.