摘要
为探讨金属硫蛋白（MT）对豚鼠乳头肌缺血再灌注损伤所致心律失常的影响，利用标准玻璃微电极技术，采用缺氧及复氧豚鼠乳头肌模型，模拟体内缺血再灌注损伤，观察不同浓度MT对豚鼠乳头肌电生理特性的影响。结果显示低浓度的MT（0．002mmol／L）对正常及缺氧和复氧豚鼠乳头肌的动作电位（AP）有关参数及自律性均无影响；中等浓度的MT（0．02mmol／L）仅使正常乳头肌的AP复极达50％时程（APD50）缩短24％（P＜0．05），但使缺氧乳头肌的AP复极达20％时程（APD20）、APD50和AP复极达90％时程（APD90）分别缩短68％、56％和43％（P均＜0．01），并使静息电位（RP）、AP幅值（APA）和0相最大上升速率（Vmax）分别增加30％、30％和45％（P均＜0．01）；高浓度的MT（0．1mmol／L）使正常豚鼠乳头肌的APD20、APD50和APD90分别缩短57％、54％和50％（P均＜0．01），并且RP、APA及Vmax分别下降22％（P＜0．05）、28％（P＜0．01）和29％（P＜0．05），而使缺氧豚鼠乳头肌的APD20、APD50和APD90分别延长92％、78％和50％（P均＜0．01），对RP、APA及Vmax无明显影响。在复氧期间，0．02mmol／L的MT可使自律性的发生率从77．8％降至55．6％（P＜0．05）；而0．1mmol／L的MT则使自律性的发生率从77.8％降至22．
To examine the effects of metallothionein (MT) on the arrhythmia caused by ischemia and reperfusionby use of standard glass microeletrode technique,effects of MT on electrophysiologic properties were studied in themold of anoxic and reoxygenated papillary muscles. Results:MT (0. 002 mmol/L) had no influence on AP normaland anoxic and reoxygenated papillary muscles;MT (0. 02 mmol/L) only shortened 24% (P<0.05 ) of APD50 ofnormal papillary muscles,but MT significantly shortened APD20 ,APD50 and APD90 of anoxic papillary muscles to68%, 56 % and 43 %, respectively, P<0. 01 ; RP, APA and Vmax increased 30%, 30%, and 45%, respectively, P<0.01; MT (0.1 mmol/L) shortened APD20,APD50,and APD90 to 57 %, 54 % and 50% of the control,respectively, P<0.01; 3RP,APA and Vmax reduced 22 % (P<0. 05), 28% (P<0.01) and 29% (P<0. 05) respectively; but MT(0.1 mmol/L) caused a prolongation in the APD20,APD50,and APD90 to 92%, 78% and 50% of the anoxic group,respectively,P<0. 01;RP,APA and Vmax had no obvious change. During reoxygenation, MT (0.02 nmol/L ) couldsignificantly decreased the automaticity of papillary muscles from 77. 8% to 55. 6% (P<0.05),when the level ofMT increased to 0.1 mmol/L, the automaticity was reduced to 22. 2 % (P<0. 01). Conclude: MT can possess aproperty of modulating intracellular Ca2+ infux.
出处
《中国心脏起搏与心电生理杂志》
1997年第3期155-158,共4页
Chinese Journal of Cardiac Pacing and Electrophysiology
