Vroman L, Adams A L, Brakman M
Haemostasis. 1985;15(5):300-3. doi: 10.1159/000215163.
Onto 'activating' surfaces, intact normal plasma deposits an overlapping sequence of proteins, each being desorbed by the next. Ultimately, high molecular weight kininogen (HMK) is deposited unless contact was too short, or space between 2 surfaces too narrow. Thus, injected between a glass slide and a convex lens, intact plasma will leave a disk of HMK with a center of fibrinogen. We describe here how the exchange of proteins on the surface can be demonstrated by staining the adsorbate with a metal oxide suspension. Subsequent flooding of the preparation with more normal plasma causes lift-off of the oxide where underlying fibrinogen is being displaced by the HMK of the newly applied plasma. Kininogen-deficient plasma fails to remove any oxide, while normal plasma can remove nearly all of the oxide and adsorbate, left on glass by HMK-deficient plasma.
在“活化”表面上，完整的正常血浆会沉积一系列重叠的蛋白质，每种蛋白质都会被下一种蛋白质解吸。最终，会沉积高分子量激肽原（HMK），除非接触时间过短，或者两个表面之间的间距过窄。因此，将完整的血浆注入载玻片和凸透镜之间，会留下一个以纤维蛋白原为中心的HMK圆盘。我们在此描述如何通过用金属氧化物悬浮液对吸附物进行染色来证明表面上蛋白质的交换。随后用更多的正常血浆冲洗制剂，会导致氧化物脱落，因为新加入血浆中的HMK正在取代下面的纤维蛋白原。缺乏激肽原的血浆无法去除任何氧化物，而正常血浆可以去除几乎所有由缺乏HMK的血浆留在玻璃上的氧化物和吸附物。
