Cattaneo M, Mustard J F, Canciani M T, Richardson M, Federici A B, Mannucci P M
A. Bianchi Bonomi Hemophilia and Thrombosis Centre, University of Milano, Italy.
Thromb Haemost. 1988 Oct 31;60(2):280-8.
We have studied the interaction of ASvWf with human platelets in PRP and in suspensions of washed platelets containing either physiological or low external ionized calcium concentration [Ca2+]o. In hirudin-PRP or in washed platelets in 1.5-2 mM CaCl2, ASvWf up to 50 micrograms/ml does not induce platelet aggregation or the release reaction. When [Ca2+]o is decreased by addition of citrate to hirudin-PRP or when no CaCl2 is added to washed platelet suspensions, ASvWf does induce platelet aggregation and the release reaction. In low [Ca2+]o, ASvWf interacts with platelet GPIb to cause primary aggregation of disc-shaped platelets to each other through GPIIb/IIIa, with or without added fibrinogen. This primary platelet aggregation leads to thromboxane A2 formation and secondary aggregation and the release reaction. With [Ca2+]o in the physiological range, there is less ASvWf interaction with GPIb, no primary platelet aggregation and no thromboxane A2 formation. The ASvWf-platelet interaction at physiological [Ca2+]o, however, enhances the platelet response to collagen or epinephrine.
我们研究了变应原性血管性血友病因子（ASvWf）与富血小板血浆（PRP）中的人血小板以及含有生理浓度或低细胞外游离钙浓度[Ca2+]o的洗涤血小板悬液之间的相互作用。在水蛭素-PRP中或在含有1.5 - 2 mM氯化钙的洗涤血小板中，高达50微克/毫升的ASvWf不会诱导血小板聚集或释放反应。当通过向水蛭素-PRP中添加柠檬酸盐来降低[Ca2+]o时，或者当未向洗涤血小板悬液中添加氯化钙时，ASvWf确实会诱导血小板聚集和释放反应。在低[Ca2+]o条件下，ASvWf与血小板糖蛋白Ib（GPIb）相互作用，通过糖蛋白IIb/IIIa（GPIIb/IIIa）使盘状血小板彼此发生初级聚集，无论是否添加纤维蛋白原。这种血小板初级聚集会导致血栓素A2形成以及次级聚集和释放反应。在[Ca2+]o处于生理范围内时，ASvWf与GPIb的相互作用较少，不会发生血小板初级聚集，也不会形成血栓素A2。然而，在生理[Ca2+]o条件下，ASvWf与血小板的相互作用会增强血小板对胶原蛋白或肾上腺素的反应。
