Effect of phosphocreatine on transient outward potassium current in ischemic ventricular mid-myocardial cells of rats

AIM: To determine the effect of exogenous phosphocreatine (PCr) at different concentrations on transient outward potassium (I_to) current in rat ischemic ventricular mid-myocardial (M) cells and to explore the antiarrhythmia mechanism in the treatment of ischemic heart disease. METHODS: M cells were isolated enzymatically from left ventricular mid-myocardium of rats. Peak I_to current was recorded by patch-clamp technique in the whole-cell configuration when M cells were superfused with normal Tyrode solution, simple ischemic solution,and simulated ischemic solution containing PCr at concentrations of 5, 10, 20 and 30 mmol/L for 10 min. RESULTS: Peak I_to current density of M cells superfused with simple simulated ischemic solution was significantly reduced by (76.1?6.3)% (P<0.05) compared with M cells superfused with Tyrode solution. Ischemic solution containing 5, 10, 20 and 30 mmol/L PCr reduced peak I_to current density by (57.1?9.6)% (P<0.05), (40.3?10.3)% (P<0.05), (34.3?9.6)% (P<0.05) and (32.1?10.6)% (P<0.05),respectively. There was statistical difference among ischemic solution without PCr and containing PCr at concentrations of 5 and 10 mmol/L groups (P<0.05). No statistical difference among groups of 10, 20 and 30 mmol/L PCr was observed (P>0.05). CONCLUSION: PCr reverses the inhibition of I_to current under ischemic condition in M cells, which may be the mechanism responsible for arrhythmia prevention in ischemic heart disease. PCr at concentrations of 0~10 mmol/L exerts significant dose-effect relationship.