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铅诱导发育中小脑微循环未成熟血管的通透性变化。

Lead-induced permeability changes in immature vessels of the developing cerebellar microcirculation.

作者信息

Press M F

出版信息

Acta Neuropathol. 1985;67(1-2):86-95. doi: 10.1007/BF00688128.

Abstract

The ultrastructure and microcirculatory permeability changes of lead encephalopathy were studied in an animal model using horseradish peroxidase as an intravascular tracer. The fine structure of capillary sprouts in the developing cerebellar microcirculation of lead-poisoned rats were described. Immature vessels, characterized by the presence of endothelial sprouts, were found to have focal areas of endothelial injury with degenerating endothelial cells. These disruptions of the microcirculatory endothelium had tracer extending from the vessel lumen to the surrounding neuropil. The degenerating endothelial cells were found as early as 24-28 h after the first administration of lead acetate by gastric lavage (2-3-day-old rats). The early injury to endothelial cells of immature vessels in the developing microcirculation is suggested as an important component of the vascular permeability changes which characterize lead encephalopathy. Older animals (5-10 days old) had microaneurysmal vascular dilatations which had a complex internal structure formed by endothelial cells. These microaneurysmally dilated vessels may represent an endothelial response to preceding endothelial injury of immature vessels.

摘要

以辣根过氧化物酶作为血管内示踪剂,在动物模型中研究了铅中毒性脑病的超微结构和微循环通透性变化。描述了铅中毒大鼠发育中小脑微循环中毛细血管芽的精细结构。以存在内皮芽为特征的未成熟血管,发现有内皮损伤的局灶区域,内皮细胞发生退变。微循环内皮的这些破坏使示踪剂从血管腔延伸至周围神经毡。最早在经胃灌洗给予醋酸铅(2 - 3日龄大鼠)后24 - 28小时就发现了退变的内皮细胞。发育中小微循环中未成熟血管内皮细胞的早期损伤被认为是铅中毒性脑病特征性血管通透性变化的一个重要组成部分。年龄较大的动物(5 - 10日龄)有微动脉瘤性血管扩张,其具有由内皮细胞形成的复杂内部结构。这些微动脉瘤性扩张的血管可能代表内皮对未成熟血管先前内皮损伤的一种反应。

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