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Procoagulant Stimulus Processing by the Intrinsic Pathway of Blood Plasma Coagulation

机译:血浆凝血固有途径的促凝血刺激加工

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Potentiation of the intrinsic pathway of human blood plasma coagulation in vitro by contact with a solidprocoagulant surface leads to bolus release of thrombin (FIIa) in concentration proportion to the intensity of activation asmeasured by procoagulant surface area or energy (water wettability). This rather remarkable finding is confirmed using twodifferent assays: one triggering coagulation substantially through the intrinsic pathway alone and the second triggeringcoagulation through the intrinsic pathway in the presence of exogenous FIIa spikes.Similarity of experimental outcomes of these assays strongly suggests that endogenous FIIa production through the intrinsicpathway is independent of the absolute amount of FIIa present in plasma. Furthermore, we corroborate previous workindicating that procoagulant surfaces remain activating after repeated use and are not poisoned or denatured in the process ofactivating plasma coagulation. It is concluded that the sharp control mechanism that gives rise to bolus-production of FIIa fromthe intrinsic pathway must occur between surface activation of FXII and the FII → FIIa step, is not related to inhibition byFIIa, and does not involve deactivation of procoagulant surfaces.
机译:通过与固体促凝剂表面接触来体外增强人血浆凝结的内在途径会导致凝血酶(FIIa)的推注释放,其浓度与通过促凝剂表面积或能量(水润湿性)测得的活化强度成比例。两种不同的测定方法证实了这一相当显着的发现:一种基本上仅通过内在途径触发凝血,第二种在存在外源FIIa尖峰的情况下通过内在途径触发凝血。内在途径与血浆中FIIa的绝对量无关。此外,我们证实以前的工作表明,促凝剂表面在反复使用后仍保持活化状态,并且在激活血浆凝结过程中不会中毒或变性。结论是,从内在途径引起FIIa推注产生的强烈控制机制必须发生在FXII的表面活化和FII→FIIa步骤之间,与FIIa的抑制作用无关,并且不涉及促凝剂表面的失活。

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