急性胰腺炎大鼠心室肌细胞瞬间外向钾电流的变化

目的探讨急性胰腺炎大鼠心室肌细胞瞬间外向钾电流的变化。方法以开腹胆总管注射牛磺胆酸钠的方法制备大白鼠急性胰腺炎实验模型，24～48h后处死动物分离单个心室肌细胞，采用全细胞膜片钳技术观察心肌细胞瞬间外向钾电流（Ito）的变化，以正常大白鼠心肌细胞的Ito为对照。结果急性胰腺炎大鼠心室肌细胞的瞬间外向钾电流受到抑制，电流密度电压关系曲线下移，其峰值电流密度由对照组的（52．16±13．12）pA／pF下降为急性胰腺炎组的（11．83±4．20）pA／pF，＋70mV的Ito电流密度较对照组下降了58．15％（P〈0．001），其失活曲线左移，半数最大失活电位对照组为（-45．2±8．3）mV，急性胰腺炎组为（-55．0±8．6）mV，与对照组比较显著减小（P〈0．001），失活速度加快；急性胰腺炎组Ito恢复速度明显减慢，恢复时程延长（与对照组比较P〈0．001）。结论急性胰腺炎后心室肌细胞的Ito受抑制，可能为急性胰腺炎后发生心律失常发生的机制之一。

Changes of transient outward potassium currents of rat of cardiac myocytes in acute pancreatitis

Objective To determine the changes of transient outward potassium currents（L） of ventricular myocytes in rat with acute pancreatitis. Methods Rat models with acute pancreatitis were made by injection of sodium taurocholate into the pancreatic duct. After 24-48 h, The animals were sacrificed and single ventricular myocyte was isolated enzymatical ly. Ito was recorded using patch clamp technique in the whole cell configuration. Results Ito from cardiac myocytes in the acute pancreatitis group was significantly reduced （ 11. 83 ± 4. 20） pA/pF] compared with the cells from control group （52.16±13. 12）pA/pF, P〈0. 001], the peak curent density decreased by 58. 15 %. The steady state inactivation curve shifted to the hyperpolarizing direction, the half-maximal voltage-dependent inactivation（V1/2 ） was （-55.0± 8.6） mV in cardiac cells from pancreatitis group and （-45.2 ± 8. 3）mV in the control cells. Ito recovered more slowly in cardiac cells from pancreatitis group than in normal cells. Conclusion Inhibitation of Ito was found in ventricular myocytes of rats with acute pancreatitis and it might be important in the development of arrythmias.