O'brien J R
Portsmouth and Isle of Wight Area Pathological Service.
J Clin Pathol. 1962 Sep;15(5):446-52. doi: 10.1136/jcp.15.5.446.
if adenosine diphosphate is added to the blood the adhesiveness of the platelets is increased and this effect is largely independent of temperature. The mono- and triphosphates decrease adhesiveness at 20 degrees C. and 37 degrees C. but have no effect at 0 degrees C.; cocaine inhibits adhesion at 37 degrees C. and at 0 degrees C. Aggregation and viscous metamorphosis of platelets in native plasma is induced at 37 degrees C. by adenosine diphosphate or by thrombin; these reactions do not occur at 0 degrees C. Cocaine and all the other anti-adhesive drugs inhibit thrombin or adenosine diphosphate-induced aggregation. The mono- and tri-phosphates appear to compete with adenosine diphosphate and inhibit aggregation; they also inhibit thrombin-induced aggregation. Aggregation induced by adenosine diphosphate or thrombin is not prevented by any of the usual enzyme inhibitors or uncoupling agents at the appropriate strength. At 37 degrees C. aggregation and viscous metamorphosis induced by adenosine diphosphate or thrombin are reversible, and the addition of more adenosine diphosphate or of thrombin again produces aggregation and viscous metamorphosis. Platelets incubated with adenosine diphosphate but not agitated lose their power to aggregate but when more adenosine diphosphate is added with agitation, then aggregation is again produced. These observations are presumably explained by the finding that intact platelets, but not fragmented platelets, can inactivate adenosine diphosphate. From these results it is tentatively concluded that adhesion may involve intrinsic adenosine diphosphate in the platelet which may be activated by thrombin and inhibited by the added mono- or triphosphate. The anti-adhesive drugs act in a different manner. These phenomena have a remarkable similarity to those concerning mitochondrial swelling.
天然血液中的血小板能自发地黏附于玻璃，且与温度无关：若向血液中添加二磷酸腺苷，血小板的黏附性会增强，且这种效应在很大程度上与温度无关。一磷酸腺苷和三磷酸腺苷在20℃和37℃时会降低黏附性，但在0℃时无此作用；可卡因在37℃和0℃时均会抑制黏附。天然血浆中血小板的聚集和黏性变形在37℃时可由二磷酸腺苷或凝血酶诱导产生；这些反应在0℃时不会发生。可卡因和所有其他抗黏附药物均会抑制凝血酶或二磷酸腺苷诱导的聚集。一磷酸腺苷和三磷酸腺苷似乎能与二磷酸腺苷竞争并抑制聚集；它们还能抑制凝血酶诱导的聚集。二磷酸腺苷或凝血酶诱导的聚集不会被任何强度合适的常用酶抑制剂或解偶联剂所阻止。在37℃时，二磷酸腺苷或凝血酶诱导的聚集和黏性变形是可逆的，添加更多的二磷酸腺苷或凝血酶会再次产生聚集和黏性变形。用二磷酸腺苷孵育但未搅拌的血小板会失去聚集能力，但搅拌下添加更多二磷酸腺苷时，又会再次产生聚集。这些观察结果大概可以通过以下发现来解释：完整的血小板而非破碎的血小板能够使二磷酸腺苷失活。从这些结果初步推断，黏附可能涉及血小板内源性二磷酸腺苷，它可能被凝血酶激活，并被添加的一磷酸腺苷或三磷酸腺苷抑制。抗黏附药物的作用方式不同。这些现象与线粒体肿胀的现象有显著相似之处。
