McPherson J, Zucker M B
Blood. 1976 Jan;47(1):55-67.
In normal heparinized blood, the retention of platelets in glass bead columns was low in the first 1 or 2 ml, increasing to more than 80% by the 4th or 5th ml. Prior flushing of the columns with platelet-poor plasma or saline lowered retention in all 5 ml. Additional studies were carried out with a two-stage procedure in which a sample of blood (A) was pumped through a column, immediately flushed out with saline or plasma, and followed by a second blood sample (B). When as little as 1 ml of blood A preceded the flushing solution, retention was very high in all 5 ml of the subsequent blood B. This enhancement of retention in B occurred, providing blood A contained platelets (other than thrombasthenic), fibrinogen, and adequate divalent cations. Enhancement did not require von Willebrand factor (vWF) in A, nor was ADP necessary, since enhancement occurred even when heparinized blood as A contained prostaglendin E1 (PGE1) or creatine phosphokinase with creatine phosphate (CPK-CP). However, the presence of PGE1 or CPK-CP in the plasma used to flush the columns prevented the enhancement of retention in the first milliliter of B. Retention in the first milliliter of B (following normal blood as A and saline or normal plasma for flushing) was high when B was afibrinogenemic, moderately high when B contained PGE1 or CPK-CP, and low in thrombasthenic, EDTA, or vWF-deficient blood. Retention declined in subsequent milliliters of PGE1 or CPK-CP blood and remained low in thrombasthenic, vWF-deficient, or EDTA blood. Our findings suggest that (1) the platelets in A adhere to glass; this adhesion requires fibrinogen but not vWF or ADP; (2) the adherent platelets release ADP and become sticky; (3) adhesion of platelets in the first milliliter of B to the sticky platelets from A requires vWF and divalent cations but not ADP; (4) retention is maintained thereafter by repetitive platelet-platelet interactions involving ADP release, alteration of adherent platelets by released ADP, and adhesion of further platelets to these ADP-altered platelets which requires vWF.
在正常肝素化血液中，玻璃珠柱对血小板的保留率在前1或2毫升血液中较低，到第4或5毫升时增加到80%以上。先用缺乏血小板的血浆或生理盐水冲洗柱子会降低所有5毫升血液中的保留率。还进行了一项两阶段程序的额外研究，即先将一份血液样本（A）泵入柱子，立即用生理盐水或血浆冲洗出来，然后再注入第二份血液样本（B）。当在冲洗液之前仅有1毫升血液A时，随后的所有5毫升血液B中的保留率都非常高。只要血液A中含有血小板（除血小板无力症患者的血小板外）、纤维蛋白原和足够的二价阳离子，血液B中的保留率就会提高。血液A中不需要血管性血友病因子（vWF），也不需要二磷酸腺苷（ADP），因为即使肝素化血液A中含有前列腺素E1（PGE1）或磷酸肌酸激酶与磷酸肌酸（CPK-CP）时，保留率也会提高。然而，用于冲洗柱子的血浆中存在PGE1或CPK-CP会阻止血液B第一毫升中的保留率提高。当血液B为无纤维蛋白原血症时，血液B第一毫升中的保留率（在血液A为正常血液且用生理盐水或正常血浆冲洗之后）很高；当血液B含有PGE1或CPK-CP时，保留率中等偏高；而在血小板无力症、乙二胺四乙酸（EDTA）或vWF缺乏的血液中保留率较低。在随后的几毫升含有PGE1或CPK-CP的血液中，保留率下降，在血小板无力症、vWF缺乏或EDTA血液中保留率仍较低。我们的研究结果表明：（1）血液A中的血小板黏附于玻璃；这种黏附需要纤维蛋白原，但不需要vWF或ADP；（2）黏附的血小板释放ADP并变得黏附性增强；（3）血液B第一毫升中的血小板与来自血液A的黏附性血小板的黏附需要vWF和二价阳离子，但不需要ADP；（4）此后，通过涉及ADP释放、释放的ADP改变黏附的血小板以及更多血小板与这些被ADP改变的血小板黏附的重复性血小板-血小板相互作用来维持保留率，而这种黏附需要vWF。
