Casonato A, Pontara E, Bertomoro A, Dannhauser D, Sartori M T, Patrassi G, Boeri G, Girolami A
University of Padua Medical School, Institute of Medical Semeiotics, Italy.
Blood Coagul Fibrinolysis. 1995 Sep;6(6):574-8. doi: 10.1097/00001721-199509000-00012.
The acute simultaneous release of tissue plasminogen activator (t-PA) and von Willebrand factor (vWF) from endothelial cells in response to a variety of agonists including thrombin, DDAVP, histamine and adrenalin has been described. In the present study we investigated the effect of venous occlusion on the circulating levels of t-PA and vWF, as well as the molecular organization of vWF in 20 normal subjects. After occlusion a significant increase in plasma t-PA levels was observed even after the values were corrected for haemoconcentration. Venous occlusion also enhanced plasma vWF values, but the increase was abolished when the correction for haemoconcentration was introduced. Following venous occlusion, no circulating abnormally large vWF multimers were detected in the subjects studied. These forms are normally not present in the circulation and are released from endothelial cells through the regulated vWF pathway; their absence therefore seems to demonstrate that this pathway is not activated after venous occlusion. Since occlusion does not enhance vWF synthesis, the increase in vWF observed in the subjects investigated may be fully attributed to haemoconcentration.
已有研究描述了内皮细胞在凝血酶、去氨加压素、组胺和肾上腺素等多种激动剂作用下，组织纤溶酶原激活物（t-PA）和血管性血友病因子（vWF）的急性同时释放。在本研究中，我们调查了静脉阻塞对20名正常受试者循环中t-PA和vWF水平以及vWF分子结构的影响。阻塞后，即使对血液浓缩进行校正，血浆t-PA水平仍显著升高。静脉阻塞也会提高血浆vWF值，但引入血液浓缩校正后，这种升高就消失了。静脉阻塞后，在所研究的受试者中未检测到循环中异常大的vWF多聚体。这些形式通常不存在于循环中，而是通过受调控的vWF途径从内皮细胞释放；因此，它们的不存在似乎表明该途径在静脉阻塞后未被激活。由于阻塞不会增强vWF合成，在研究的受试者中观察到的vWF增加可能完全归因于血液浓缩。
