摘要
目的探讨急性胰腺炎后心肌细胞快钠通道的变化。方法以开腹胰管内注射牛磺胆酸钠的方法制备大白鼠急性胰腺炎实验模型,24-48 h后处死动物分离单个心室肌细胞,采用全细胞膜片钳记录技术观察心肌细胞快钠通道电流(INa)的变化,同时设假手术对照组。结果急性胰腺炎大鼠心室肌细胞的快钠电流受到抑制,电流密度-电压关系曲线上移,其峰值电流密度:对照组为(-13．55± 5．33)pA/pF,急性胰腺炎组为(-6．80±2．03)pA/pF,较对照组下降了49．82％,P<0．001;其失活曲线左移,半数最大失活电位对照组为(-105±21)mV;急性胰腺炎组为(-121±26)mv,与对照组比较显著减小,P<0．01,失活速度加快;急性胰腺炎组INa恢复速度明显减慢,恢复时程延长,和对照组比较P<0． 01。结论急性胰腺炎后心室肌细胞的快钠通道受抑制,细胞兴奋性及传导速度下降,可能为急性胰腺炎后发生心律失常的机制之一。
Objective To determine the changes of sodium currents （INa） of rat ventricular myocytes after acute pancreatitis. Methods Rat models with acute pancreatitis were made by injection of sodium taurocholate into the pancreatic duct. After 24 to 48 hours, single ventricular myocytes were isolated enzymatically, INa were recorded by using patch clamp techniques in the whole cell configuration. Results Peak of INa from ventricular myocytes in the acute pancreatitis group was significantly reduced （ - 6.80 pA/pF ± 2.03 pA/pF） compared to cells from control group （ - 13.55 pMpF ± 5.33 pMpF）, P 〈 0.001, the peak decreased 49.82%. The steady-state inactivation curve was shifted to the hyperpolarizing direction, the half-maximal voltage dependence of inactivation （V1/2） was （ - 121 ± 26） mV in ventricular cells from pancreatitis group and （ - 105 ± 21） mV in the control cells. INa recovered more slowly in cardiac cells from pancreatitis group than normal cells. Conclusion Inhibitation of INa is found in ventricular myocytes and might be important in the development of arrythmias in rats with acute pancreatitis.
出处
《白求恩军医学院学报》
2005年第4期193-195,共3页
Journal of Bethune Military Medical College
关键词
大鼠
急性胰腺炎
心肌细胞
膜片钳
钠通道
Rat
Acute pancreatitis
Cardiomyocyte
Patch clamp
Sodium current
