急性胰腺炎后心肌细胞快钠通道的变化

Changes of sodium channel of ventricular cells after acute pancreatitis

目的探讨急性胰腺炎后心肌细胞快钠通道电流(I_(Na))的变化。方法开腹胆总管注射牛磺胆酸钠制备大白鼠急性胰腺炎模型,24 h后处死动物分离单个心室肌细胞,用膜片钳术记录I_(Na)。结果急性胰腺炎大鼠心室肌细胞的I_(Na)受到抑制,I—V曲线上移,峰值电流密度明显下降[(-6．80±2．03)pA/pF vs(-13．55±5．33)pA/pF,P＜0．001]；失活曲线左移,急性胰腺炎组V_(0．5)显著减小[(-121±26)mv vs (-105±21)mV,P＜0．001]；急性胰腺炎组I_(Na)失活后再恢复明显减慢(P＜0．01)。结论急性胰腺炎后心室肌细胞的快钠通道受抑制,可能为急性胰腺炎后发生心律失常发生的机制之一。

Objective To study the changes of sodium currents （INa） of ventricular eells in rats after acute pancreatitis. Methods Rats＇ models of acute pancreatitis were produced by injecting sodium taurocholate into the pancreatic duct. After 24 hours, single ventricular cells was isolated enzymatically, and INa were recorded by using patch clamp techniques. Results INa peak from ventricular cells in the acute pancreatitis group was significantly reduced （ - 6.80± 2.03） pA/pF compared with that in control group （ - 13.55± 5.33） pA/pF, P 〈 0.001. The steady-state inactivation curve was shifted to upward direction, the half-maximal voltage dependence of inactivation （ V0.5 ） was （ - 121 ± 26） mV in ventricular cells from pancreatitis group and （ - 105 ± 21 ） mV form the control group,INa returned to normal more slowly in ventricular cells from panereatitis group than that from control group. Conclusion Inhibitation of INa was found in ventrlcular cells, whieh might cause arrhythmias in rats with acute pancreatitis.