Blezer R, Cahalan L, Cahalan P T, Lindhout T
Department of Biochemistry, Cardiovascular Research Institute, Maastricht University, The Netherlands.
Blood Coagul Fibrinolysis. 1998 Jul;9(5):435-40. doi: 10.1097/00001721-199807000-00006.
In the present study we used an in-vitro technique to examine initiation and propagation of blood coagulation at the surface of tantalum coronary stents exposed to flowing platelet-rich and platelet-free plasma. The time course of factor IXa production at the surface of the stent was not influenced by platelets. In spite of a significant factor IXa production, no thrombin activity was detected when the tantalum stent was exposed to platelet-free plasma; only when the stent was exposed to platelet-rich plasma was extensive thrombin production observed. These findings indicate that tantalum triggers blood coagulation, but that (adherent) platelets are essential for thrombin generation. Heparin-coated tantalum stents exposed to flowing platelet-rich plasma showed that factor IXa generation was slightly reduced compared with the bare stent. However, the heparin coating drastically delayed the onset of thrombin generation and largely reduced the steady-state production of thrombin. We found a clear relationship between the antithrombin binding capacity and the antithrombogenic potential of the heparin-coated stents. The mode of action of immobilized heparin is thought to abrogate thrombin generation by inhibiting thrombin-dependent positive feedback reactions at the surface of the coronary stent.
在本研究中，我们采用体外技术，研究富血小板血浆和无血小板血浆流经钽冠状动脉支架表面时凝血的起始和传播情况。支架表面因子IXa生成的时间进程不受血小板影响。尽管有显著的因子IXa生成，但当钽支架暴露于无血小板血浆时，未检测到凝血酶活性；只有当支架暴露于富血小板血浆时，才观察到大量凝血酶生成。这些发现表明，钽触发血液凝固，但（黏附的）血小板对于凝血酶生成至关重要。暴露于流动富血小板血浆的肝素涂层钽支架显示，与裸支架相比，因子IXa生成略有减少。然而，肝素涂层极大地延迟了凝血酶生成的起始，并在很大程度上降低了凝血酶的稳态生成。我们发现肝素涂层支架的抗凝血酶结合能力与其抗血栓形成潜力之间存在明显关系。固定化肝素的作用方式被认为是通过抑制冠状动脉支架表面的凝血酶依赖性正反馈反应来消除凝血酶生成。
