Addonizio V P, Colman R W
Biomaterials. 1982 Jan;3(1):9-15. doi: 10.1016/0142-9612(82)90054-0.
Extensive contact between blood and the synthetic surfaces of an extra-corporeal circuit causes thrombocytopenia, release of platelet granular contents, initiation of thromboxane synthesis, disruption of subcellular architecture and loss of platelet sensitivity to standard platelet agonists. All too frequently, these adverse platelet alterations are reflected in a prolongation of the post-operative bleeding time and excessive blood loss which precludes implementation of long-term circulatory assist devices. Unfortunately, a truly biocompatible material does not exist and efficiency of gas transport demands haemodynamic designs which actually promote platelet injury. Although manipulation of surface properties and mechanical improvements in circuitry have managed to reduce platelet-surface interactions, the ultimate potential of these manoeuvres may be limited. Synthetic surfaces and soluble agonists, however, appear to modulate similar pathways suggesting that temporary platelet inhibition might provide significant protection by preserving the morphological and functional integrity of circulating platelets during contact with extracorporeal circuits.
血液与体外循环的合成表面广泛接触会导致血小板减少、血小板颗粒内容物释放、血栓素合成启动、亚细胞结构破坏以及血小板对标准血小板激动剂的敏感性丧失。这些不良的血小板改变常常表现为术后出血时间延长和失血过多，从而妨碍了长期循环辅助装置的应用。不幸的是，目前不存在真正具有生物相容性的材料，而气体传输效率要求采用实际上会促进血小板损伤的血液动力学设计。尽管表面特性的操控和回路的机械改进已设法减少了血小板与表面的相互作用，但这些操作的最终潜力可能有限。然而，合成表面和可溶性激动剂似乎调节相似的途径，这表明在与体外循环接触期间，通过保持循环血小板的形态和功能完整性，暂时抑制血小板可能会提供显著的保护作用。
