Copley A L
Thromb Res Suppl. 1983;5:105-45.
The author's theory of the endoendothelial fibrin lining (EEFL), first advanced in 1953 and developed by him ever since, localizes the homeostasis between steady fibrin formation and deposition, or 'fibrination', and continuous fibrinolysis in the more or less immobile portion of the plasmatic zone next to the vessel wall. In 1971, the author advanced, in relation to the EEFL, the theory of fibrinogen gel clotting without thrombin action or 'fibrinogenin' formation in vivo. Considerable direct and indirect experimental evidence, secured by the author and by several other investigators, advanced markedly the knowledge of the normal physiology and the pathophysiology of various disease processes involving the vessel wall and blood circulation. The information presented is an extension to that given in the author's recent overview (Clin. Hemorheology 1, 9-72, 1981). It deals both with new data by several investigators including those by the author, as well as with older data from the literature. The author maintained already in 1960 that the blood together with the blood vessels, in which it circulates, constitute 'an entity'. In 1981 he postulated this entity to be a very special organ, named conveniently 'vessel-blood organ', which is ubiquitous and penetrates all other organs and adjacent tissues. The EEFL of the vessel-blood organ is considered by the author as the crucial critical interface between the blood and the vessel wall. It is the primary barrier, followed by the endothelium (comprising the endothelial cells and the interendothelial cement substance which contains or is identical with 'cement fibrin') and the basement membrane for the exchanges between the blood, the vessel wall and its surrounding tissues and spaces. The EEFL acts as anticoagulant, is antithrombogenic, maintains vascular patency and aids cardiac action by decreasing significantly the apparent viscosity of blood, referred to in the literature as the 'Copley-Scott Blair phenomenon'. A new concept of leukocyte emigration traversing the capillary wall is presented, affecting focal fibrinolysis of the EEFL and of fibrin contained in the interendothelial cement substance and in the basement membrane. The physical property of capillary (or vascular) permeability is related to the existence of the EEFL, since, as found by Copley et al, both fibrinopeptides, liberated in the transition of fibrinogen to fibrin, and plasminopeptides, freed in the conversion of plasminogen to plasmin, enhance capillary permeability. Capillary fragility, which is antagonistic to capillary permeability, is in great part due to fibrinolytic action on fibrin as a constituent of the basement membrane.(ABSTRACT TRUNCATED AT 400 WORDS)
作者的血管内皮纤维蛋白衬里(EEFL)理论于1953年首次提出,此后一直由他不断完善。该理论认为,在紧邻血管壁的血浆区域相对静止的部分,稳定的纤维蛋白形成与沉积(即“纤维蛋白化”)和持续的纤维蛋白溶解之间的稳态得以维持。1971年,作者针对EEFL提出了纤维蛋白原凝胶在无凝血酶作用下凝结或体内形成“纤维蛋白原素”的理论。作者以及其他几位研究人员获取的大量直接和间接实验证据,显著推进了我们对涉及血管壁和血液循环的各种疾病过程的正常生理学和病理生理学的认识。本文所呈现的信息是对作者近期综述(《临床血液流变学》1, 9 - 72, 1981)内容的扩展。它既涉及包括作者在内的几位研究人员的新数据,也涉及文献中的旧数据。作者早在1960年就认为血液及其循环的血管构成了“一个实体”。1981年,他假定这个实体是一个非常特殊的器官,方便地命名为“血管 - 血液器官”,它无处不在,穿透所有其他器官和相邻组织。作者认为血管 - 血液器官的EEFL是血液与血管壁之间的关键界面。它是血液、血管壁及其周围组织和空间进行物质交换的主要屏障,其次是内皮(包括内皮细胞和内皮间胶状物质,其中含有或等同于“胶状纤维蛋白”)和基底膜。EEFL具有抗凝作用,抗血栓形成,维持血管通畅,并通过显著降低血液的表观粘度来辅助心脏活动,文献中称此为“科普利 - 斯科特·布莱尔现象”。本文提出了白细胞穿越毛细血管壁迁移的新概念,这一过程会影响EEFL以及内皮间胶状物质和基底膜中所含纤维蛋白的局部纤维蛋白溶解。毛细血管(或血管)通透性的物理特性与EEFL 的存在有关,因为正如科普利等人所发现的,纤维蛋白原转化为纤维蛋白过程中释放的纤维蛋白肽以及纤溶酶原转化为纤溶酶过程中释放的纤溶酶肽都会增强毛细血管通透性。与毛细血管通透性相反的毛细血管脆性,在很大程度上归因于纤维蛋白溶解对作为基底膜成分的纤维蛋白的作用。(摘要截选至400字)