Vairel E G, Bouty-Boye H, Toulemonde F, Doutremepuich C, Marsh N A, Gaffney P J
Thromb Res. 1983 May 1;30(3):219-24. doi: 10.1016/0049-3848(83)90075-0.
In human volunteers unfractionated heparin and a low molecular weight fraction of heparin (LMWH) caused an increase in plasma plasminogen activator (PA) which peaked at 3 hours after subcutaneous injection. Using a perfused isolated rabbit ear model the enhancement of PA activity was confirmed and was related to the anti-Xa activity of both products infused. Using a modified rabbit Wessler model for thrombus formation it was found that, when using doses of heparin and LMWH sufficient to give a 100% antithrombotic effect, antifibrinolytic drugs (eg. epsilon-ACA and aprotinin), negated this protective effect. It is concluded that the effect of heparin and LMWH on haemostasis is mediated in part through the enhancement which these drugs have on fibrinolysis, the latter being arguably a major defence against fibrin formation during thrombosis.
在人类志愿者中,普通肝素和低分子量肝素(LMWH)可使血浆纤溶酶原激活剂(PA)增加,皮下注射后3小时达到峰值。使用灌注离体兔耳模型证实了PA活性的增强,且与注入的两种产品的抗Xa活性相关。使用改良的兔韦氏勒血栓形成模型发现,当使用足以产生100%抗血栓作用剂量的肝素和LMWH时,抗纤溶药物(如ε-氨基己酸和抑肽酶)会抵消这种保护作用。得出的结论是,肝素和LMWH对止血的作用部分是通过这些药物对纤溶的增强作用介导的,后者可以说是血栓形成过程中对抗纤维蛋白形成的主要防御机制。