尼卡地平可减轻海葵毒素II诱导的离体大鼠和猪心脏冠状动脉血流量的减少。
Nicardipine diminished equinatoxin II-induced decrease of coronary flow in isolated rat and pig hearts.
作者信息
Bunc Matjaz, Rozman Janez, Vidmar Alenka, Rakovec Peter, Drevensek Gorazd, Budihna Metka V, Suput Dusan
机构信息
Department of Patophysiology, Zalozka 4, Medical Faculty, Ljublana, Slovenia.
出版信息
Cell Mol Biol Lett. 2002;7(2):355-7.
Equinatoxin II (EqT II) is a basic, cardiotoxic polypeptide. The vasoconstrictory effect of the toxin on isolated porcine coronary arteries was diminished by nicardipine, an L-type calcium channel antagonist. A comparison was made of the effects of EqT II alone and EqT II in the presence of nicardipine on the coronary flow in porcine and rat hearts isolated according to Langendorff's method. In both models EqT II decreased coronary flow in a dose-dependent manner and there were no statistically significant differences between the two models (p>0.05). However, 1 M nicardipine diminished the effects of EqT II on coronary flow in isolated porcine hearts more than in isolated rat hearts (p<0.05). The results suggest that the activation of L-type calcium channels is one of the mechanisms involved in the lowering of coronary flow induced by EqT II.
海葵毒素II（EqT II）是一种碱性心脏毒性多肽。L型钙通道拮抗剂尼卡地平可减弱该毒素对离体猪冠状动脉的血管收缩作用。比较了单独使用EqT II以及在尼卡地平存在的情况下EqT II对按照Langendorff法分离的猪和大鼠心脏冠脉血流的影响。在两种模型中，EqT II均以剂量依赖方式降低冠脉血流，且两种模型之间无统计学显著差异（p>0.05）。然而，1 μM尼卡地平对EqT II降低离体猪心脏冠脉血流的作用的减弱程度大于对离体大鼠心脏的作用（p<0.05）。结果表明，L型钙通道的激活是EqT II诱导冠脉血流降低所涉及的机制之一。
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