Thomopoulos G N, Spicer S S, Gratton M A, Schulte B A
Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston 29425, USA.
Hear Res. 1997 Sep;111(1-2):31-41. doi: 10.1016/s0378-5955(97)00080-4.
Ultrastructural examination was undertaken to investigate the pathogenesis of age-related atrophy of the stria vascularis (StV). Basement membrane (BM) thickness was increased in 65-85% of strial capillaries in gerbils aged 33 months or older and often exceeded by several-fold that observed in young controls. In an early stage of thickening the BM expanded slightly around the full capillary profile, after which nodular expansions of BM encircling slender cell processes were often observed at or near one or both poles of the elliptical vessel profile. As widening progressed, the BM consisted of 2-3 layers separated by cell processes in the nodules but fewer strata elsewhere. Association of slender processes of both endothelial cells and pericytes with focal thickening outside the process suggested their participation in genesis of the capillary lesion. In later stages of atrophy, pericytes degenerated and disappeared, while endothelial cells remained intact. Eventually, thick multilayered BM devoid of endothelial cells surrounded a narrow lumen occluded by debris. The age-related change in BM in the inner ear was confined to StV capillaries. Degenerative changes in StV epithelial cells occurred apparently as a secondary consequence of the capillary lesion. The pathologic alterations in marginal cells included extrusion of blebs from the luminal surface, separation and loss of basolateral interfoldings, alteration and depletion of mitochondria and nuclear pyknosis. At the end-stage of degeneration, the StV consisted of a simple or multiple layer of squamous cells lining the scala media.
进行超微结构检查以研究血管纹(StV)年龄相关性萎缩的发病机制。在33个月及以上的沙鼠中,65%-85%的血管纹毛细血管基底膜(BM)厚度增加,且常常超过年轻对照几倍。在增厚的早期阶段,BM围绕整个毛细血管轮廓略有扩张,之后在椭圆形血管轮廓的一极或两极处或其附近,常可见到BM围绕细长细胞突起的结节状扩张。随着增宽进展,BM在结节处由被细胞突起分隔的2-3层组成,而其他部位层数较少。内皮细胞和周细胞的细长突起与突起外的局灶性增厚相关,提示它们参与了毛细血管病变的发生。在萎缩的后期,周细胞退化并消失,而内皮细胞保持完整。最终,由多层厚的无内皮细胞的BM围绕着一个被碎片阻塞的狭窄管腔。内耳BM的年龄相关性变化局限于血管纹毛细血管。血管纹上皮细胞的退行性变化显然是毛细血管病变的继发结果。边缘细胞的病理改变包括从腔面挤出泡状突起、基底外侧褶的分离和丧失、线粒体的改变和耗竭以及核固缩。在退化的末期,血管纹由单层或多层衬于中阶的鳞状细胞组成。