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人脑水肿中人类皮质毛细血管基底膜的超微结构改变。

Ultrastructural alterations of human cortical capillary basement membrane in human brain oedema.

作者信息

Castejón Orlando José

机构信息

Prof. Orlando José Castejón, MD, Biological Research Institute, Faculty of Medicine, Zulia University, Maracaibo, Venezuela, fax: 58-261-7831611, e-mail:

出版信息

Folia Neuropathol. 2014;52(1):10-21. doi: 10.5114/fn.2014.41740.

Abstract

The capillary basement membranes are examined in severe traumatic brain injuries, vascular malformation, congenital hydrocephalus and brain tumours. They exhibit homogeneous and nodular thickening, vacuolization, rarefaction, reduplication, and deposition of collagen fibers. Their average thickness varied according to the aetiology and severity of brain oedema. In moderate brain oedema the thickness ranged from 71.97 to 191.90 nm in width, and in patients with severe brain oedema it varied from 206.66 to 404.22 nm. The basement membrane complex appears apparently intact in moderate oedema, and shows glio-basal dissociation in severe oedema. In areas of highly increased cerebro-vascular permeability, the basement membrane shows matrix disorganization, reduplication, and bifurcations protruding toward the endothelial cells, and acting as abluminal transcapillary channels. In regions of total brain necrosis, its structural stability is lost showing loosening, dissolution and rupture. Basement membrane swelling is due to overhydration of its protein-complex glycoprotein matrix. The thickening, rarefaction and vacuolization are induced by the increased vacuolar and vesicular transendothelial transport. The degenerated basement membrane areas exhibit a finely granular precipitate interpreted as protein, proteoglycan, glycoprotein, and agrin degraded matrix.

摘要

在严重创伤性脑损伤、血管畸形、先天性脑积水和脑肿瘤中对毛细血管基底膜进行检查。它们表现出均匀和结节状增厚、空泡化、稀疏、重复以及胶原纤维沉积。其平均厚度根据脑水肿的病因和严重程度而有所不同。在中度脑水肿中,厚度范围为71.97至191.90纳米宽,而在重度脑水肿患者中,厚度范围为206.66至404.22纳米。基底膜复合物在中度水肿中显然完整,而在重度水肿中显示神经胶质 - 基底解离。在脑血管通透性高度增加的区域,基底膜显示基质紊乱、重复以及向内皮细胞突出的分支,并作为管腔外跨毛细血管通道。在全脑坏死区域,其结构稳定性丧失,表现为松弛、溶解和破裂。基底膜肿胀是由于其蛋白质 - 复合糖蛋白基质的过度水化所致。增厚、稀疏和空泡化是由增加的空泡和囊泡跨内皮运输诱导的。退化的基底膜区域呈现出细颗粒状沉淀物,被解释为蛋白质、蛋白聚糖、糖蛋白和聚集蛋白降解的基质。

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