Sills A K, Clatterbuck R E, Thompson R C, Cohen P L, Tamargo R J
Hunterian Neurosurgical Laboratory, Department of Neurosurgery, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Neurosurgery. 1997 Aug;41(2):453-60; discussion 460-1. doi: 10.1097/00006123-199708000-00025.
The exposure of large intracranial arteries to blood after an aneurysmal subarachnoid hemorrhage leads to a cascade of morphological and physiological changes in the vessels, a condition generally described as vasospasm. This response to the periadventitial deposition of blood is mediated in part by the endothelial layer of the vessel. This study was undertaken to examine the role of endothelial cell expression of intercellular adhesion molecule 1 (ICAM-1) in the initiation and regulation of this response.
The femoral artery model of vasospasm was used in rats (65 animals, 130 arteries). In each rat, one artery was exposed to blood and the contralateral vessel was exposed to saline, so that each animal served as its own control. Animals were perfused and killed at sequential time points, from 1 hour to 20 days after blood exposure. The vessels were examined immunohistochemically and histologically for the presence of ICAM-1 and morphological features of vasospasm, respectively.
Endothelial cell ICAM-1 immunoreactivity was extensively increased in only the blood-exposed vessels, beginning 3 hours after clot placement and persisting for 24 hours. ICAM-1 immunoreactivity returned to baseline by 48 hours after blood exposure. The influx of inflammatory cells correlated directly with the time and location of increased ICAM-1 expression. Peak arterial remodeling was observed on the blood-exposed side 8 to 12 days after clot placement, as quantified by measurements of increased wall thickness, decreased lumen size, and increased collagen content.
Endothelial cell ICAM-1 expression seems to be an early and specific signal used by a vessel in response to the deposition of blood periadventitially. This molecule may be a marker for vessels likely to undergo subsequent morphological remodeling and vasospasm.
动脉瘤性蛛网膜下腔出血后，颅内大动脉暴露于血液中会导致血管发生一系列形态和生理变化，这种情况通常被称为血管痉挛。血管外膜周围血液沉积引发的这种反应部分是由血管内皮介导的。本研究旨在探讨细胞间黏附分子1（ICAM-1）在内皮细胞中的表达在这种反应的起始和调节中的作用。
采用大鼠血管痉挛的股动脉模型（65只动物，130条动脉）。在每只大鼠中，一条动脉暴露于血液中，对侧血管暴露于盐水中，因此每只动物自身作为对照。在血液暴露后1小时至20天的连续时间点对动物进行灌注并处死。分别通过免疫组织化学和组织学检查血管中ICAM-1的存在情况以及血管痉挛的形态学特征。
仅在暴露于血液的血管中，内皮细胞ICAM-1免疫反应性在血凝块放置后3小时开始广泛增加，并持续24小时。血液暴露后48小时，ICAM-1免疫反应性恢复至基线水平。炎性细胞的流入与ICAM-1表达增加的时间和位置直接相关。通过测量血管壁厚度增加、管腔尺寸减小和胶原蛋白含量增加来量化，在血凝块放置后8至12天，在暴露于血液的一侧观察到动脉重塑的峰值。
内皮细胞ICAM-1表达似乎是血管对血管外膜周围血液沉积作出反应时使用的一种早期特异性信号。该分子可能是可能经历后续形态重塑和血管痉挛的血管的标志物。
