血管移植的病理学。

K M Müller, G Dasbach
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引用次数: 31

摘要

为了分析聚四氟乙烯和涤纶合成假体在动脉系统中的掺入模式,对手术切除的21个假体和尸检获得的7个假体进行了检查;植入时间从30分钟到10年不等。本质上,假体植入的早期阶段(I期)包括作为急性炎症过程一部分的渗出性炎症反应。组织结构的有序程度以及基质和细胞在反应中的相互影响似乎很小。假体外表面的细胞浸润是局部起源的,而假体内层含有造血起源的细胞。组织期(II期),类似于炎症反应的修复-增殖期,网状内皮系统被激活,同时开始吞噬和假体结构变薄。在假体细胞渗透过程中,ⅰ型、ⅲ型胶原蛋白和纤维连接蛋白对细胞既起到引导作用,又起到生长通道的作用。纤维连接蛋白和III型胶原蛋白具有特殊的“催化”功能。I型胶原蛋白使血管假体在假体周围组织中牢固地锚定。由于纤维被吞噬而导致的假体稳定性的丧失被血管壁内新形成的结缔组织所平衡。参与组织的成纤维细胞必须来源于流动的血液和局部间充质细胞。慢性炎症反应在晚期持续存在。在某些情况下,观察到假体内间充质衬里的增殖增加并伴有退行性变化。血管管腔侧缺乏连续的周围基质结构可被认为是这种增生的主要原因。未见造血细胞转化为成血管细胞或内皮细胞。小的内皮化区域仅在吻合口附近和经假体血管渗透后可见。
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The pathology of vascular grafts.

In order to analyse the incorporation pattern of synthetic prosthesis made of Teflon and Dacron in the arterial system, 21 prostheses removed surgically and seven prostheses obtained from autopsies were examined; the duration of the implantation periods ranged from 30 min up to 10 years. Essentially the early phase of prosthetic incorporation (phase I) includes exudative inflammatory reactions as part of acute inflammatory processes. The degree of order within the tissue architecture and the mutual influence of matrix and cells in the reaction appeared to be slight. The cellular infiltrate found on the outer prosthetic surface is of local origin whereas the inner prosthetic lining contains cells of haematogenous origin. The organisation phase (phase II), which is comparable to the reparative-proliferative phase of an inflammatory reaction, showed activation of the reticulo-endothelial system together with the start of phagocytosis and a thinning of the prosthetic structures. Collagen type I and type III and fibronectin served both as a guidance and a growth tract for the cells during the cellular permeation of the prosthesis. Fibronectin and collagen type III have a special "catalytic" function. Collagen type I causes the firm anchoring of the vascular prosthesis in the periprosthetic tissue. The loss of stability of the prosthesis due to phagocytosis of fibres is balanced by the newly formed connective tissue within the wall of the vessel. The fibroblasts involved in the organisation must be derived from the flowing blood and from local mesenchymal cells. A chronic inflammatory reaction persisted during the late phase. In some cases increased proliferation of the inner mesenchymal lining of the prosthesis was observed together with regressive changes. The lack of a continuous surrounding stromal architecture on the luminal side of the vessel can be regarded as the main reason for this proliferation. Transformation of haematogenous cells into angioblasts or endothelial cells was not seen. Small endothelialised areas were only seen in the vicinity of anastomoses and following transprosthetic permeation by capillaries.

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