肺动脉内膜外植体通透性与内皮层结构的关系。

Federation proceedings Pub Date : 1987-06-01
B Meyrick, E A Perkett, T R Harris, K L Brigham
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引用次数: 0

摘要

血管通透性的改变与内皮细胞的结构损伤有关。这些功能和结构的变化可以通过实验产生,并使用牛肺动脉内膜外植体进行检测。功能与结构变化的相关性使我们能够解剖内皮损伤的机制。我们已经证明,用组胺孵育内膜外植体会导致内皮间扩张的短暂形成,并增加了氚化水和[14C]蔗糖在内膜外植体中的平衡率。暴露于内毒素也会引起内皮间扩张,但内皮损伤比组胺更严重,体内实验显示肺血管通透性增加的时间更长。白细胞迁移也被认为会导致内皮层屏障功能下降。用内皮细胞和分离的牛白细胞进行的实验表明,跨内皮细胞的迁移可能依赖于趋化刺激。无论是粒细胞向酶酶酶激活的血浆迁移,还是淋巴细胞向淋巴细胞条件培养基(RPMI,其中淋巴细胞与豆豆蛋白A孵育)迁移,都不会导致外植体通透性的可检测性增加,但粒细胞向淋巴细胞条件培养基的迁移确实会导致[14C]蔗糖的平衡增加。最后,一个理论模型被用来检验暴露于组胺的内膜外植体的通透性变化。该模型由两个隔间组成,放射性示踪剂通过已知渗透率的过滤器扩散。这样的模型与在完整绵羊中获得的数据很好地吻合,表明数学模型可以定量估计内膜外植体中的屏障功能,与体内数据相比更有利。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Correlation of permeability with the structure of the endothelial layer of pulmonary artery intimal explants.

Changes in vascular permeability are associated with structural damage to endothelial cells. These functional and structural changes can be produced experimentally and examined by using intimal explants from bovine pulmonary artery. Correlation of functional with structural changes allows us to dissect the mechanisms responsible for endothelial damage. We have shown that incubation of intimal explants with histamine causes transient formation of interendothelial dilatations and an increased rate of equilibration of tritiated water and [14C]sucrose across the intimal explant. Exposure to endotoxin also causes interendothelial dilatations but the endothelial damage is more severe than that with histamine, and in vivo experiments show a more prolonged increase in pulmonary vascular permeability. Leukocyte migration has also been suggested to result in a decreased barrier function of the endothelial layer. Experiments with the endothelial layer of intimal explants and separated bovine leukocytes suggest that transendothelial migration may depend on the chemotactic stimulus. Neither granulocyte migration toward zymosan-activated plasma nor lymphocyte migration toward lymphocyte-conditioned medium (RPMI in which lymphocytes were incubated with concanavalin A) leads to detectable increases in explant permeability, but granulocyte migration toward lymphocyte-conditioned medium does result in increased equilibration of [14C]sucrose. Finally, a theoretical model has been used to examine the permeability changes seen for the intimal explants exposed to histamine. The model consists of two compartments with radioactive tracers diffusing across a filter of known permeability. Such a model gives good agreement with data obtained in intact sheep, indicating that mathematical models allow quantitative estimates of barrier function in intimal explants that compare favorably with in vivo data.

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