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风湿热时心肌变性,随后发生细胞转化、再生和纤维生成。

Degeneration of cardiac muscle followed by cell transformation, regeneration and fibrogenesis in rheumatic fever.

作者信息

McDonald H G, Calkins H E

出版信息

Exp Pathol (Jena). 1978;15(4):185-95. doi: 10.1016/s0014-4908(78)80055-6.

Abstract

In acute rheumatic fever, various types of myocardial degeneration and subsequent transformation of the damaged muscle fibers into a variety of cells, classified and unclassified, are described from microscopic examination of autopsy specimens. This study suggests that in the origin of Aschoff bodies, the diagnostic feature of rheumatic fever, there are three different pathways (Types A, B and C) for cytogenesis of Aschoff cells from altered muscle fibers. Type A cytogenesis takes place through the stage of Anitschkow myocytes of cardiac muscle origin (McDONALD 1963), and the Type B pathway, through the stage of dedifferentiated cells arising in lysing cardiac muscle fibers. These dedifferentiated cells with capacity for regeneration of regular cardiac muscle fibers (McDONALD 1975), show abortive or atypical development of muscle cells through the Aschoff cell stage. The Type C cytogenesis of Aschoff cells takes place through direct transformation of cardiac muscle fibers which show central hyalinization of myoplasm and changes in nuclei from normal to single or multinucleated large vesicular forms. The fibrinoid material of Aschoff bodies is shown to be the product of muscle origin. The mechanism of formation of fibrous scars in the myocardium and fibrous thickening of subendocardium are explained on the basis of fibrous transformation of cardiac muscle. Altered muscle fibers have been shown to give rise to cells which simulate inflammatory cells and others which cannot be classified.

摘要

在急性风湿热中,通过对尸检标本的显微镜检查,描述了各种类型的心肌变性以及随后受损肌纤维向多种已分类和未分类细胞的转化。本研究表明,在风湿热的诊断特征——阿绍夫小体的起源中,从改变的肌纤维产生阿绍夫细胞有三种不同的细胞发生途径(A、B和C型)。A型细胞发生通过心肌来源的阿尼奇科夫心肌细胞阶段(麦克唐纳,1963年),B型途径则通过溶解的心肌纤维中产生的去分化细胞阶段。这些具有正常心肌纤维再生能力的去分化细胞(麦克唐纳,1975年),通过阿绍夫细胞阶段显示出肌细胞的发育异常或不典型。阿绍夫细胞的C型细胞发生通过心肌纤维的直接转化发生,这些心肌纤维显示肌浆中央透明变性以及细胞核从正常变为单个或多核大泡状形式。阿绍夫小体的纤维蛋白样物质被证明是肌肉来源的产物。基于心肌的纤维性转化,解释了心肌纤维性瘢痕形成和心内膜下纤维性增厚的机制。已显示改变的肌纤维可产生模拟炎症细胞的细胞以及其他无法分类的细胞。

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