Cooper H A, Wilkins K W, Johnson P R, Wagner R H
J Lab Clin Med. 1977 Sep;90(3):512-21.
Platelet-aggregating factor (PAF) was removed from bovine plasma by human platelets fixed with 2% formaldehyde. The degree of adsorption was directly related to the platelet concentration and the length of incubation. Fixed washed platelets (FWP) aggregated with bovine plasma could be deaggregated by 1M KCl, Evans blue, and 8M urea but not by beta-galactosidase. Incubation with 1M KCl eluted some but not all of the PAF, as the deaggregated platelets spontaneously aggregated upon removal of the deaggregating conditions. Also, fixed platelets adsorbed PAF even in the presence of 1M salt or after treatment with Evans blue. Platelet aggregation was not affected by thrombin (20 micron/ml) but was abolished by trypsin at concentrations as low as 4 X 10(-1) microgram/ml. The data suggest that deaggregation is not the result of elution of the loosely bound aggregating factor from the platelet surface, but rather the disruption of noncovalent interplatelet bridging between one or more PAF molecules bound to a specific receptor.
用2%甲醛固定的人血小板从牛血浆中去除血小板聚集因子(PAF)。吸附程度与血小板浓度和孵育时间直接相关。与牛血浆聚集的固定洗涤血小板(FWP)可被1M KCl、伊文思蓝和8M尿素解聚,但不能被β-半乳糖苷酶解聚。用1M KCl孵育洗脱了部分而非全部PAF,因为去除解聚条件后解聚的血小板会自发聚集。此外,即使在1M盐存在下或用伊文思蓝处理后,固定血小板仍能吸附PAF。凝血酶(20微克/毫升)不影响血小板聚集,但浓度低至4×10⁻¹微克/毫升的胰蛋白酶可消除血小板聚集。数据表明,解聚不是从血小板表面洗脱松散结合的聚集因子的结果,而是与特定受体结合的一个或多个PAF分子之间非共价血小板间桥接的破坏。