Drevensek G, Budihna M V, Suput D, Bunc M
Dept. of Pharmacol. & Exp. Toxicol., Ljubljana, Slovenia.
Pflugers Arch. 2000;440(5 Suppl):R145-6.
Death after i.v. administration of equinatoxin II (EqT II) has been attributed to the circulatory failure resulting from cardiotoxic effects. The mechanism of action is unknown. The aim of the present work was to study the effects of the toxin on vascular tone in the isolated porcine coronary artery and on coronary flow in the isolated pig heart. EqT II caused concentration-dependent contractions of rings of the isolated epicardial porcine coronary artery with an EC50 value of 89+/-5 nM (n=5-6) and maximal effect of about 140% of the contraction induced by 20 nM KCl. On Langendorffs porcine heart preparation EqT II caused a dose-dependent decrease of coronary flow. At EqT II doses lower than 0.05 micromol/100 g of heart weight there were no measurable effects of the toxin. At dose 0.5 micromol/100 g the toxin decreased coronary flow to less than 9.8+/-2.5% of the control value. The constrictory effect of the toxin on isolated porcine coronary arteries was diminished by the L-type calcium channel antagonist nicardipine (NC). NC in 1 microM concentration almost completely abolished the effect of EqT II on coronary flow. Our results confirmed involvement of L-type calcium channels in the vasoconstrictory effects of EqT II on epicardial coronary arteries.
静脉注射海葵毒素II（EqT II）后的死亡归因于心脏毒性作用导致的循环衰竭。其作用机制尚不清楚。本研究的目的是研究该毒素对离体猪冠状动脉血管张力以及离体猪心脏冠脉流量的影响。EqT II可引起离体猪心外膜冠状动脉环的浓度依赖性收缩，其半数有效浓度（EC50）值为89±5 nM（n = 5 - 6），最大效应约为20 nM氯化钾诱导收缩的140%。在Langendorff猪心脏标本上，EqT II可引起冠脉流量的剂量依赖性降低。当EqT II剂量低于0.05 μmol/100 g心脏重量时，该毒素无明显可测效应。当剂量为0.5 μmol/100 g时，该毒素可使冠脉流量降至对照值的9.8±2.5%以下。L型钙通道拮抗剂尼卡地平（NC）可减弱该毒素对离体猪冠状动脉的收缩作用。1 μM浓度的NC几乎完全消除了EqT II对冠脉流量的影响。我们的结果证实L型钙通道参与了EqT II对心外膜冠状动脉的血管收缩作用。
