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海葵毒素II降低离体大鼠心脏冠脉血流量取决于细胞外钙离子浓度。

Lowering of the coronary flow in isolated rat heart by equinatoxin II depends upon extracellular Ca2+ concentration.

作者信息

Drevensek G, Bunc M, Budihna M V, Suput D

机构信息

Department of Pharmacology and Experimental Toxicology, Medical Faculty, Ljubljana, Slovenia.

出版信息

Pflugers Arch. 2000;439(3 Suppl):R150-1.

Abstract

Equinatoxin II (EqT II) is a basic polypeptide toxin from the sea anemone Actinia equina (L.). Its LD50 in mice is 33 g/kg. The cause of death after intravenous application has been attributed to the circulatory failure resulting in the cardiotoxic effects. In Langendorff's rat and guinea-pig heart preparations EqT II caused dose dependent decrease in the coronary flow (CF). Morphologic changes of different cell cultures incubated with EqT II are the result of Ca2+ entry through the newly formed discrete pores. Pores in the cell membranes are composed of the toxin oligomeres. In the present study we tried to evaluate the dependence of vasoconstrictor effects of EqT II on isolated rat hearts upon the Ca2+ concentration in the perfusion solution. EqT II did not affect the CF in the group without Ca2+. The strongest effect was observed in the group with 1.5 mM Ca2+ where the CF decreased to 7.7+/-7%. The results of our experiments indicate that the effects of EqT II on CF depend on Ca2+ concentration in the extracellular solution.

摘要

海葵毒素II(EqT II)是一种来自马海葵(Actinia equina (L.))的碱性多肽毒素。其对小鼠的半数致死量为33微克/千克。静脉注射后导致死亡的原因被认为是循环衰竭引起的心脏毒性作用。在Langendorff大鼠和豚鼠心脏标本中,EqT II可导致冠状动脉血流量(CF)呈剂量依赖性减少。用EqT II孵育不同细胞培养物后的形态学变化是钙离子通过新形成的离散孔道进入细胞的结果。细胞膜上的孔道由毒素寡聚体组成。在本研究中,我们试图评估EqT II对离体大鼠心脏的血管收缩作用对灌注液中钙离子浓度的依赖性。在无钙离子的组中,EqT II不影响冠状动脉血流量。在钙离子浓度为1.5毫摩尔/升的组中观察到最强的作用,此时冠状动脉血流量降至7.7±7%。我们的实验结果表明,EqT II对冠状动脉血流量的影响取决于细胞外溶液中的钙离子浓度。

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