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结缔组织疾病病变发病机制中血管通透性增加的研究:I. 实验性高脂血症与免疫性关节病

Studies on increased vascular permeability in the pathogenesis of lesions of connective tissue diseases: I. Experimental hyperlipidaemia and immune arthropathy.

作者信息

Valente A J, Walton K W

出版信息

Ann Rheum Dis. 1980 Oct;39(5):490-9. doi: 10.1136/ard.39.5.490.

DOI:10.1136/ard.39.5.490
PMID:7436581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1000592/
Abstract

In order to investigate the known associations between hyperlipidaemia and various rheumatic complaints, immune arthritis and hyperlipidaemia have been induced concurrently in rabbits. The results obtained show that: (1) Rabbit apolipoprotein B-containing lipoproteins (LpB), which are normally virtually excluded from joint fluid, gain access to the inflamed joint in the serous effusion and serve as intrinsic indicators of altered local permeability to macromolecules. (2) Much of the LpB entering the joint space is taken up by the phagocytic cells and, following intracellular hydrolysis, leaves a lipid residue. In some chronically affected joints these residues are modified so as to give rise to crystalline cholesterol and its esters. Such crystals may serve as a chronic irritant in the joint. (3) In addition intact LpB is found sequestered in the superficial layers of intra-articular collagenous structures of the challenged joint in a distribution identical with that of similarly sequestered immune complexes and complement, suggesting altered permeability of these intra-articular structures also.

摘要

为了研究高脂血症与各种风湿性病症之间已知的关联,已在兔身上同时诱发免疫性关节炎和高脂血症。获得的结果表明:(1) 兔含载脂蛋白B的脂蛋白 (LpB),正常情况下实际上无法进入关节液,但在浆液性渗出液中可进入发炎关节,并作为局部对大分子通透性改变的内在指标。(2) 进入关节腔的大部分LpB被吞噬细胞摄取,细胞内水解后留下脂质残渣。在一些长期受累的关节中,这些残渣发生改变,从而产生结晶胆固醇及其酯类。此类晶体可能在关节中起慢性刺激物的作用。(3) 此外,发现完整的LpB隔离在受攻击关节的关节内胶原结构表层,其分布与同样被隔离的免疫复合物和补体相同,这也表明这些关节内结构的通透性发生了改变。

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ANTIGEN-ANTIBODY CROSSED ELECTROPHORESIS.抗原-抗体交叉电泳
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Increased arterial collagen synthesis in experimental canine atherosclerosis.实验性犬动脉粥样硬化中动脉胶原合成增加。
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The pathogenesis of xanthomata.黄瘤的发病机制。
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The pathogenesis of chronic inflammation in experimental antigen-induced arthritis. II. Preferential localization of antigen-antibody complexes to collagenous tissues.实验性抗原诱导性关节炎中慢性炎症的发病机制。II. 抗原-抗体复合物在胶原组织中的优先定位。
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