Effect of phosphocreatine on transient outward potassium current in ischemic ventricular mid-myocardial cells of rats
10.3969/j.issn.1000-4718.2012.04.006
- VernacularTitle:磷酸肌酸对缺血大鼠心室中层心肌细胞瞬间外向钾电流的影响
- Author:
Xiangmin SHI
;
Tiande LI
;
Yutang WANG
;
Zhaoliang SHAN
;
Tingshu YANG
- Publication Type:Journal Article
- Keywords:
Patch-clamp techniques;
Transient outward potassium current;
Ischemia;
M cells;
Phosphocreatine;
Rats
- From:
Chinese Journal of Pathophysiology
2012;28(4):608-612
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To determine the effect of exogenous phosphocreatine (PCr) at different concentrations on transient outward potassium (Ito) 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 Ito 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 Ito 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 Ito 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 Ito 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.
