类α-蝎神经毒素BmKⅠ对离体大鼠心脏收缩力及电活动的特异调控(英文)  

BmK I,an α-like scorpion neurotoxin, specifically modulates isolated rat cardiac mechanical and electrical activity

作　　者：孙海英[1] 朱海峰[1] 吉永华[1] 

机构地区：[1]中国科学院上海生命科学研究院上海生理研究所,上海200031

出　　处：《生理学报》2003年第5期530-534,共5页Acta Physiologica Sinica

基　　金：This work was supported by National Basic Research Priorities Program of China (1999054001), partially grants from National Nature Sciences Foundation of China (39625010).

摘　　要：本研究探讨了一种特异性钠通道调制剂(Buthus martensi Karsch,BmK I)对离体大鼠心脏收缩力及电活动的调制作用。离体心脏灌流实验显示:(1)BmK I(0.5-10μmol/L)剂量依赖地增强大鼠心肌收缩力,左心室最大发展压(LVDP_(max))以及dp/dt_(max) 。与对照组相比均显著增强(n=6,P<0.05),同时可触发正性变时作用(n=6,P<0.05);(2)大剂量BmK I(20μmol/L)引起负性肌力作用及心动过缓;(3)冠脉流量随心脏收缩力的增强反而减小,应用500nmol/L BmK I时冠脉流量由14.5ml/min降至8.6ml/min(n=6,P<0.05);此外,心电图记录表明 BmK I(0.5-10μmol/L)可触发心动过速及复杂的心律失常等电活动变化;正常灌流液洗脱后BmK I引起的大鼠心脏收缩力及电活动的改变可部分恢复。由于β-肾上腺素能受体阻滞剂普奈洛尔预先应用抑制了儿茶酚胺类神经递质的释放,提示BmK I引起的大鼠心脏收缩力及电活动的改变不是由于其调节儿茶酚胺类神经递质的释放及随后β-肾上腺素能受体的激活,而可能与其对心肌电压门控钠通道的调控有关。In this study, cardiotonic and cardiotoxic effects of Buthus martensi Karsch (BmK) I, a modulator of voltage-ga-ted sodium channels, were investigated on the isolated rat hearts. The results showed that BmK I evoked complex effects charac-terized by a change in both cardiac mechanical and electrical activity. Langendorff perfusion showed that: (1 ) maximal left ven-tricular developed pressure (LVDP_(max)) and dp/dt_(max) were markedly increased by BmK I (0. 5 - 10 μmol/L) in a dose-depend-ent manner (n = 6, P<0. 05 ), positive chronotropic effects were also induced by BmK I (n = 6, P<0. 05 ); (2 ) negative ino-tropic action and bradycardia could be elicited at a larger dose of BmK I (20 μmol/L); (3 ) the coronary flow varied inverselywith the positive inotropic effects, coronary flow reduced during positive inotropic effects from 14. 5 to 8. 6 ml/min after adminis-tration of 500 nmol/L BmK I (n = 6, P<0. 05 ). In addition, tachycardia and complex cardiac arrhythmias were induced byBmK I (0. 5 - 10 μmol/L). The modulating of BmK I on the heart mechanical, electrical activity could be partially recoveredafter washing. As propranolol was applied to block the release of catecholamines before administration of BmK I, suggesting thatthe changes in cardiac mechanical and electrical activity induced by BmK I might not due to catecholamine release from the nerveterminal and subsequent stimulation of the β-adrenoceptor but attributable to the modulation of BmK I on cardiac voltage-gatedsodium channels.

关 键 词：肌力作用 心电图 BMK Ⅰ 电压门控钠通道 

分 类 号：Q463[生物学—生理学]