Bragin M A, Cherkasov A P
Arkh Patol. 1979;41(2):46-52.
Ultrastructural examinations of 32 cases of various forms of fibrousmuscular dysplasia (FMD) of renal arteries showed the lesions at the subcellular level to be identical in all these forms and to differ only in their intensity and localization. As the disease progresses, smooth muscle cells (SMC) show signs of activation accompanied by an increased collagen synthesis. In this, the cells exhibit large multiblade nuclei, intensive proliferation of the granular endoplasmic reticulum, hypertrophy of the Golgi complex. In cases of intensive fibrous changes, occasional fibroblasts appear in the arterial media. As collagen accumulates in intercellular spaces, signs of involution of various degrees are found in SMC. The number of elastic fibers in the media of the affected arteries decreases markedly as compared with the control. The inner elastic membrane of the arteries is frequently destroyed, particularly in the intimal form of the lesions. The study suggests that all forms of FMD represent a single process in the morphogenesis of which the leading role is played by fibroblast-like transformation of SMC.
对32例各种形式的肾动脉纤维肌发育异常(FMD)进行超微结构检查发现,所有这些形式的病变在亚细胞水平上是相同的,只是强度和定位有所不同。随着疾病进展,平滑肌细胞(SMC)表现出活化迹象,伴有胶原合成增加。在此过程中,细胞呈现大的多叶核、颗粒内质网的强烈增殖、高尔基体复合体肥大。在纤维变化强烈的病例中,动脉中膜偶尔会出现成纤维细胞。随着胶原在细胞间隙中积累,SMC出现不同程度的退化迹象。与对照组相比,受累动脉中膜的弹性纤维数量明显减少。动脉的内弹性膜经常遭到破坏,尤其是在病变的内膜形式中。该研究表明,所有形式的FMD代表一个单一过程,在其形态发生中,SMC的成纤维细胞样转化起主导作用。