钙流拮抗药对眼镜蛇心脏毒升高大鼠心肌胞浆Ca~（2＋）作用的影响

Ｆｕｒａ－２荧光测定实验显示，眼镜蛇心脏毒（ＣＴＸ）能明显升高新鲜分离的大鼠心肌细胞的胞浆Ｃａ２＋浓度。维拉帕米在完全阻断高Ｋ＋引起胞浆Ｃａ２＋升高的浓度下（１μｍｏｌ·Ｌ－１）．能明显抑制ＣＴＸ作用，但不能阻断之。１．５μｍｏｌ·Ｌ－１ＣＴＸ使离体大鼠Ｌａｎｇｅｎｄｏｒｆｆ心脏收缩幅度逐渐减少，最后心脏停搏于收缩期。维拉帕米及硝苯吡啶均能明显延长心脏的搏动时间，但不能阻止ＣＴＸ引起的心脏停搏。结果提示，ＣＴＸ引起膜去极化使电位依赖性Ｃａ２＋通道开放不是ＣＴＸ触发Ｃａ２＋内流的唯一机理。

Effects of Ca￣(2+) entry blockers on the increase of cytoplasmic free Ca￣(2+) by cardiotoxin in rat heart cells

In this study, the fura-2 fluorescent technique was used to determine the effects of Ca2+ entry blockers on the increase of cytoplasmic free Ca2+ concentration induced by cardiotoxin(CTX) in freshly isolated rat heart cells.10μmol·L-1 CTX significantly increased the cytoplasmic free Ca2+. This effect of CTX was inhibited,but not Completely blocked,by 1μmol·L-1 verapamil which completely blocked the Ca2+ entry induced by 100 mmol·L-1 KCl.In Langendorff isolated heart perfusion experiment,CTX progressively inhibited heart beat until its stop.Both of verapamil and nifedipine in the concentration of 0.1μmol·L-1 markedly prolonged the duration of heart beat,but did not protected the heart from failure induced by CTX.These results suggest that the Ca2+ entry induced by CTX may be involved in other mechanisms besides the opening of voltage-dependent Ca2+ Channel evoked by CTX-induced membrane depolarization.Supported by The National Natural Science Foundation of China No.38970836