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安静老龄沙鼠的螺旋韧带病理学

Spiral ligament pathology in quiet-aged gerbils.

作者信息

Spicer Samuel S, Schulte Bradley A

机构信息

Department of Pathology and Laboratory Medicine, Medical University of South Carolina, 165 Ashley Avenue, Charleston, SC 29425, USA.

出版信息

Hear Res. 2002 Oct;172(1-2):172-85. doi: 10.1016/s0378-5955(02)00581-6.

Abstract

The ultrastructure of the spiral ligament was compared in aged and young gerbils to assess the involvement of connective tissues in the lateral wall and particularly the fibrocytes in development of presbyacusis. Pathologic features in fibrocytes of senescent gerbils spanned a wide range reflecting different stages of lateral wall involution. All of the type II, IV and V fibrocytes selectively developed cytosolic vacuoles in an early degenerative phase showing minimal strial involvement. Clear spaces indicative of interstitial edema separated the vacuolated cell bodies and their plasmalemmal processes. As a presumed intermediate phase, profiles of amorphous substance apparently derived from apoptosis/necrosis of type II fibrocytes infiltrated the type II fibrocyte area among nearly normal appearing cells. In cochlear turns with advanced strial degeneration, type II fibrocytes disappeared from the spiral prominence area leaving only type I-like fibrocytes occasionally accompanied by a collagen infiltrate. Type V fibrocytes disappeared similarly from the suprastrial area. The extent of atrophy in type II fibrocytes corresponded in general with that in the neighboring stria vascularis. Age-dependent atrophy in the lateral wall largely spared type I fibrocytes except that they often enclosed discrete amorphous foci lacking organelles. The involution thus affected principally the Na,K-ATPase-positive fibrocytes functioning in active uptake rather than passive conductance of K(+). The vacuolization and degeneration exclusive to ATPase-rich fibrocytes and the associated intercellular edema are interpreted as secondary responses, possibly as a result of impaired diffusion of K(+) through downstream marginal cells.

摘要

比较老年沙鼠和幼年沙鼠螺旋韧带的超微结构,以评估结缔组织在耳蜗外侧壁中的作用,特别是成纤维细胞在老年性聋发病过程中的作用。衰老沙鼠成纤维细胞的病理特征范围广泛,反映了外侧壁退化的不同阶段。所有II型、IV型和V型成纤维细胞在早期退化阶段选择性地出现胞质空泡,此时血管纹受累最小。空泡化的细胞体及其质膜突起被提示间质水肿的透明间隙分隔开。作为一个假定的中间阶段,明显源自II型成纤维细胞凋亡/坏死的无定形物质轮廓,在外观近乎正常的细胞中浸润II型成纤维细胞区域。在血管纹严重退化的耳蜗螺旋中,II型成纤维细胞从螺旋隆起区域消失,仅留下偶尔伴有胶原浸润的I型样成纤维细胞。V型成纤维细胞也同样从血管纹上方区域消失。II型成纤维细胞的萎缩程度总体上与相邻血管纹的萎缩程度相对应。外侧壁的年龄依赖性萎缩在很大程度上未累及I型成纤维细胞,只是它们常常包裹着缺乏细胞器的离散无定形病灶。因此,退化主要影响在钾离子主动摄取而非被动传导中起作用的钠钾ATP酶阳性成纤维细胞。富含ATP酶的成纤维细胞特有的空泡化和退化以及相关的细胞间水肿被解释为继发反应,可能是由于钾离子通过下游边缘细胞的扩散受损所致。

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