Objective To investigate the effect of exhaustive exercise on sodium channel currents (I_Na), ECG and echocardiography parameters in a rat swimming model. Methods Rats of the exercise group were forced to swim until exhaustion each time for 9 days with 5% body weight (workload) attached to the head. A swimming session will be held at 9 am from day 1 to day 9. The criteria of exhausting exercise included the rotatingmotion in water, the significant decrease in motor coordination, and more than 10 seconds from water submerged the nose to the body resurfaced. After 1 day of recovery period, we performed ventricular myocytes isolation and used whole cell patch-clamp technique to investigate sodium channel currents, sedentary rats served as controls. In addition, echocardiography and ECG parameters were analyzed. Results After 9 days of swimming exercise, a decrease in EF and FS% was observed, however, no significant differences were found between sedentary and exercise group. In addition, no significant differences were found in heart rate, LVPWs, LVPWd, IVSs, IVSd, LVIDs, LVIDd, EDV, LV Mass between sedentary and exercise group. The following ECGs parameters were increased: P wave amplitude, P wave duration, QRS amplitude and R wave amplitude, while the other parameters remained unchanged. When compared to sedentary, peak I_Na density was enhanced by exhaustive exercise, however, exhaustive exercise didn't change the steady-state activation and inactivation of I_Na. Conclusion The P, QRS and R-wave amplitudes increased after exhaustive exercise indicating impaired myocardial depolarization, which may be caused by the enhanced I_Na. These changes could shorten the action potential, and thus may contribute to proarrhythmia in cardiomyocytes.

Objective: To observe the effects of non-ionic hypoosmotic contrast agent, iopromide on ion channels in ventricular myocytes. Methods: The ventricular myocytes were isolated and whole cell patch-clamp technique was used to record the current density, steady-state activation curve and inactivation curve of sodium current (I_Na), L-type calcium current (I_Ca,L) and instantaneous outward potassium ion current (I_to) before and after iopromide administration. Results: Compared with that before iopromide administration, the current density of I_Na and I_Ca,L decreased obviously, the current density of I_to increased obviously after iopromide administration. While iopromide has no obviously effects on steady-state activation curve and inactivation curve. Conclusions: Iopromide may induce malignant ventricular arrhythmia by changing the duration of action potential of ventricular myocytes.