Levi M, ten Cate J W, Dooijewaard G, Sturk A, Brommer E J, Agnelli G
Centre for Thrombosis, Hemostasis and Atherosclerosis Research, University of Amsterdam, The Netherlands.
Thromb Haemost. 1989 Sep 29;62(2):686-9.
The desamino-d-arginine vasopressin (DDAVP) induced enhancement of endogenous fibrinolysis is generally attributed to the release of tissue-type plasminogen activator (t-PA) from the vessel wall. The observation of concurrent release of urokinase-type plasminogen activator (u-PA), which eventually might cooperate in the enhanced fibrinolytic activity, has not been reported thus far. In a preliminary study in two healthy human volunteers we found a 1.8-fold increase of urokinase-antigen (UK-antigen) and a 1.7-fold increase of plasmin-activatable pro-urokinase (pro-UK) activity to DDAVP intravenously. The plasma-peak levels coincided with the maximal t-PA level. These responses following infusion of DDAVP were subsequently confirmed in a randomized double blind cross-over study in six human volunteers. We conclude that u-PA is released by DDAVP concurrently with t-PA and that it is presumably from the same origin as t-PA i.e. endothelial cells. u-PA and t-PA may therefore cooperate in the enhanced fibrinolytic activity upon DDAVP infusion.
去氨基-D-精氨酸血管加压素(DDAVP)诱导的内源性纤溶增强通常归因于血管壁释放组织型纤溶酶原激活物(t-PA)。尿激酶型纤溶酶原激活物(u-PA)同时释放的观察结果,最终可能协同增强纤溶活性,但迄今为止尚未见报道。在对两名健康人类志愿者的初步研究中,我们发现静脉注射DDAVP后,尿激酶抗原(UK-抗原)增加了1.8倍,纤溶酶可激活的尿激酶原(pro-UK)活性增加了1.7倍。血浆峰值水平与最大t-PA水平一致。随后在一项对六名人类志愿者的随机双盲交叉研究中证实了注射DDAVP后的这些反应。我们得出结论,DDAVP与t-PA同时释放u-PA,并且推测其与t-PA来源相同,即内皮细胞。因此,u-PA和t-PA可能在注射DDAVP后协同增强纤溶活性。