Castejón O J
Instituto de Investigaciones Biológicas, Facultad de Medicina, Universidad del Zulia, Maracaibo, Venezuela.
J Submicrosc Cytol Pathol. 1988 Jul;20(3):519-36.
The fine structural alterations of cortical capillary basement membrane have been studied in 16 patients with perifocal edema associated to brain tumors, traumatic injuries complicated with subdural or epidural hematoma or hygroma and congenital malformations, such as hydrocephalus, Arnold-Chiari and Alport's syndromes and vascular anomalies. The basement membrane displayed homogeneous and nodular thickening, vacuolization, rarefaction and reduplication. Its average thickness varied according to the etiology and severity of brain edema. In nine patients with moderate brain edema the thickness ranged from 71.97 to 191.90 nm and in the remaining seven patients with severe brain edema it varied from 206.66 to 404.22 nm. The basement membrane complex appeared apparently intact in moderate edema and showed glio-basal dissociation in severe edema. In areas of highly increased cerebro-vascular permeability, the basement membrane showed matrix disorganization and bifurcations acting as abluminal transcapillary channels. In regions of total brain necrosis, its structural stability was lost showing loosening, dissolution and rupture. Proliferation of collagen fibers was also found in three cases. Basement membrane swelling was interpreted as an overhydration of its matrix. The thickening, rarefaction and vacuolization seem to be induced by the increased vacuolar and vesicular transendothelial transport. The degenerated areas feature a finely granular precipitate interpreted as a protein or glycoprotein degraded matrix.
对16例伴有局灶性水肿的患者的皮质毛细血管基底膜的超微结构改变进行了研究,这些患者患有脑肿瘤、伴有硬膜下或硬膜外血肿或脑脊膜膨出的创伤性损伤以及先天性畸形,如脑积水、阿诺德-奇亚里畸形、阿尔波特综合征和血管异常。基底膜呈现均匀和结节状增厚、空泡化、稀疏化和重复。其平均厚度根据脑水肿的病因和严重程度而有所不同。在9例中度脑水肿患者中,厚度范围为71.97至191.90纳米,其余7例严重脑水肿患者的厚度范围为206.66至404.22纳米。基底膜复合物在中度水肿时似乎完好无损,在严重水肿时显示神经胶质-基底膜分离。在脑血管通透性高度增加的区域,基底膜显示基质紊乱和分支,形成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,表现为松散、溶解和破裂。在3例中还发现了胶原纤维增生。基底膜肿胀被解释为其基质的过度水化。增厚、稀疏化和空泡化似乎是由增加的液泡和囊泡跨内皮运输诱导的。退化区域的特征是有精细颗粒状沉淀物,被解释为蛋白质或糖蛋白降解的基质。