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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。
Fura-2 fluorescence assay showed that CTX significantly increased cytosolic Ca2 + concentrations in freshly isolated rat cardiomyocytes. Verapamil completely blocked the high K + -induced increase in cytoplasmic Ca2 + (1 μmol·L-1). Can significantly inhibit the role of CTX, but can not be blocked. 1.5μmol·L-1CTX isolated rat Langendorff cardiac contractility decreased gradually, and finally cardiac arrest in systole. Both verapamil and nifedipine significantly prolonged heart beat time but did not prevent CTX-induced cardiac arrest. The results suggest that CTX induced membrane depolarization to make potential-dependent Ca2 + channels open is not the only mechanism of CTX trigger Ca2 + influx.