Barnhart M I
Mol Cell Biochem. 1978 Dec 22;22(2-3):113-37. doi: 10.1007/BF00496238.
This article summarizes recent ultrastructure findings from our laboratory and documents some of the information accumulated primarily since 1975 from many laboratories. Special attention is given to documentation by scanning electron microscopy which affords insight into platelet activation (adhesion, aggregation, release/secretion) and especially platelet-vessel wall interactions. Structural physiology of platelets is considered in some detail as a basis for understanding platelet disorders contributing to clinical problems of thrombosis and hemorrhage. The impaired ability of von Willebrand platelets to adhere to injured vessel wall is reported using the human umbilical vein perfusion model. Relationships between platelets and blood coagulation factors focus on the exquisite sensitivity of platelets to minute amounts of thrombin. Unmasking of platelet factor 3 sites is identified on activated platelets, after glutaraldehyde fixation, by their reaction ot latex bearing anti-platelet factor 3 markers. The basis for platelet-collagen interactions is reviewed. Conditions for and possible mechanisms behind platelet interaction with vessel wall are discussed. Ex vivo flowing blood-vessel wall models offer opportunities for improved understanding of the platelets role(s) in vascular diseases.
本文总结了我们实验室最近的超微结构研究结果,并记录了主要自1975年以来许多实验室积累的一些信息。特别关注扫描电子显微镜的记录,它能深入了解血小板活化(黏附、聚集、释放/分泌),尤其是血小板与血管壁的相互作用。血小板的结构生理学被详细讨论,作为理解导致血栓形成和出血等临床问题的血小板疾病的基础。使用人脐静脉灌注模型报告了血管性血友病血小板黏附于受损血管壁的能力受损。血小板与血液凝固因子之间的关系集中在血小板对微量凝血酶的高度敏感性上。在戊二醛固定后,通过活化血小板与带有抗血小板因子3标记的乳胶的反应,鉴定出血小板因子3位点的暴露。综述了血小板与胶原蛋白相互作用的基础。讨论了血小板与血管壁相互作用的条件和可能机制。体外流动血液-血管壁模型为更好地理解血小板在血管疾病中的作用提供了机会。