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纤维蛋白原和低密度脂蛋白在兔主动脉和脑动脉中的渗透与沉积——免疫电子显微镜研究

Permeation and deposition of fibrinogen and low-density lipoprotein in the aorta and cerebral artery of rabbits--immuno-electron microscopic study.

作者信息

Kurozumi T, Imamura T, Tanaka K, Yae Y, Koga S

出版信息

Br J Exp Pathol. 1984 Jun;65(3):355-64.

PMID:6743533
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2040975/
Abstract

The localization of fibrinogen and low-density lipoprotein (LDL) in the arterial wall has been studied to determine whether they mediate the effects of hypertension and/or hypercholesteraemia on atherogenesis. In untreated control rabbits, fibrinogen was localized in the caveolae and vesicles of the endothelial cells and in the subendothelial spaces of the aorta. No fibrinogen was found in the subendothelial spaces of the cerebral artery. Hypertension or hypercholesteraemia was accompanied by enhanced insudation of fibrinogen into the subendothelial spaces of the aorta and cerebral artery, and fibrinogen deposition was most prominent in the hypercholesteraemic rabbits with induced renovascular hypertension. The insudation of fibrinogen appeared to occur by way of vesicular transport, and to some extent by junctional transport. In the untreated control rabbits, LDL was localized only in the caveolae and vesicles of endothelial cells in both aorta and cerebral artery. LDL was deposited in the subendothelial space of the aorta of hypercholesteraemic rabbits with or without hypertension, and in the cerebral artery of hypercholesteraemic rabbits with hypertension. These findings suggest that fibrinogen insudates into the intima of the aorta and cerebral artery both during hypertension and hypercholesteraemia, and that LDL insudation into the intima of the aorta in hypercholesteraemia is accentuated by hypertension. LDL insudated into the intima of the cerebral artery in the presence of hypercholesteraemia linked to hypertension. Thus, hypertension plays a significant role in the pathogenesis of cerebral atherosclerosis.

摘要

对动脉壁中纤维蛋白原和低密度脂蛋白(LDL)的定位进行了研究,以确定它们是否介导高血压和/或高胆固醇血症对动脉粥样硬化形成的影响。在未经治疗的对照兔中,纤维蛋白原定位于内皮细胞的小窝和囊泡以及主动脉的内皮下间隙。在脑动脉的内皮下间隙未发现纤维蛋白原。高血压或高胆固醇血症伴有纤维蛋白原向主动脉和脑动脉内皮下间隙的渗出增加,并且在诱导肾血管性高血压的高胆固醇血症兔中纤维蛋白原沉积最为明显。纤维蛋白原的渗出似乎通过囊泡运输方式发生,并且在一定程度上通过连接运输发生。在未经治疗的对照兔中,LDL仅定位于主动脉和脑动脉内皮细胞的小窝和囊泡中。LDL沉积在有或无高血压的高胆固醇血症兔的主动脉内皮下间隙以及有高血压的高胆固醇血症兔的脑动脉中。这些发现表明,在高血压和高胆固醇血症期间,纤维蛋白原渗入主动脉和脑动脉内膜,并且高血压加剧了高胆固醇血症时LDL渗入主动脉内膜的情况。在与高血压相关的高胆固醇血症存在的情况下,LDL渗入脑动脉内膜。因此,高血压在脑动脉粥样硬化的发病机制中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/74fcb2c1d339/brjexppathol00093-0078-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/9f99ca63e89f/brjexppathol00093-0074-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/3900b6c8e0d8/brjexppathol00093-0075-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/aca12344cea3/brjexppathol00093-0076-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/7f14949d17f3/brjexppathol00093-0076-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/cabf200e22e7/brjexppathol00093-0077-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/74fcb2c1d339/brjexppathol00093-0078-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/9f99ca63e89f/brjexppathol00093-0074-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/3900b6c8e0d8/brjexppathol00093-0075-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/aca12344cea3/brjexppathol00093-0076-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/7f14949d17f3/brjexppathol00093-0076-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/cabf200e22e7/brjexppathol00093-0077-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d360/2040975/74fcb2c1d339/brjexppathol00093-0078-a.jpg

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