Huang S J, Kwan C Y
Department of Physiology, Faculty of Medicine, University of Hong Kong, Pokfulam, Hong Kong.
Res Commun Mol Pathol Pharmacol. 1996 Oct;94(1):103-10.
The effects of cardiotoxin isolated and purified from the venom of Naja naja atra on the platelet aggregation were investigated using washed rat platelets prepared chromatographically. In the presence of 1 mM Ca2+, cardiotoxin concentration-dependently induced aggregation of platelets. While extracellular Ca2+ was necessary for the induction of aggregation by cardiotoxin, high concentration of Ca2+ (e.g., 5 mM) prevented cardiotoxin-induced aggregation. Cardiotoxin-induced platelet aggregation was also blocked by 1 mM Ni2+ but not by 100 microM indomethacin or 1 microM nifedipine, indicating that cardiotoxin-induced platelet aggregation involved Ca(2+)-entry pathway other than L-type Ca2+ channels. High concentration of Ca2+ may prevent cardiotoxin-induced aggregation by competing with cardiotoxin for binding site on the platelet membranes.
采用色谱法制备的洗涤大鼠血小板，研究了从眼镜蛇毒中分离纯化的心脏毒素对血小板聚集的影响。在存在1 mM Ca2+的情况下，心脏毒素浓度依赖性地诱导血小板聚集。虽然细胞外Ca2+对于心脏毒素诱导的聚集是必需的，但高浓度的Ca2+（例如5 mM）可阻止心脏毒素诱导的聚集。1 mM Ni2+也可阻断心脏毒素诱导的血小板聚集，但100 microM吲哚美辛或1 microM硝苯地平则不能，这表明心脏毒素诱导的血小板聚集涉及L型Ca2+通道以外的Ca(2+)内流途径。高浓度的Ca2+可能通过与心脏毒素竞争血小板膜上的结合位点来阻止心脏毒素诱导的聚集。
