ICAM-1 and VCAM-1 expression following aneurysmal subarachnoid hemorrhage and their possible role in the pathophysiology of subsequent ischemic deficits
ICAM-1 and VCAM-1 expression following aneurysmal subarachnoid hemorrhage and their possible role in the pathophysiology of subsequent ischemic deficits
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DOI：
10.1159/000093243
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发表时间：
2006-01-01
影响因子：
2.9
通讯作者：
Pina, Ana-Luisa
中科院分区：
文献类型：
--
作者：
Rothoerl, Ralf Dirk;Schebesch, Karl-Michael;Pina, Ana-Luisa
背景：对蛛网膜下腔出血（SAH）后缺血性脑损伤的病理生理学了解甚少。越来越多的证据表明，炎症反应可能参与了这种延迟发生的缺血性病变的发病机制。本研究的目的是评估SAH后这些病变的粘附分子。研究方法：SAH后第9天，每天从15例患者中采集血清和脑脊液（CSF）样本，并评估细胞间粘附分子-1（ICAM-1）和血管粘附分子-1（VCAM- 1）。结果：几乎在整个时间过程中，CSF和血清样本相关性良好（p < 0.0001）。血清和CSF中ICAM-1和VCAM- 1的继发性升高与经颅多普勒血流速度的增加相关（p > 0.0001和p < 0.007），但与CT扫描中的延迟病变无关。结论：我们认为炎症过程参与了脑血管痉挛的发病机制，但它们可能只是多因素发病机制的一部分。版权所有（c）2006 S. Karger AG，巴塞尔
Background: The pathophysiology of ischemic cerebral lesions following aneurysmal subarachnoid hemorrhage ( SAH) is poorly understood. There is growing evidence that inflammatory reactions could be involved in the pathogenesis of such delayed occurring ischemic lesions. The aim of this study was to evaluate adhesion molecules with regard to these lesions following SAH. Methods: Serum and cerebrospinal fluid ( CSF) samples were taken daily from 15 patients up to day 9 after SAH and evaluated for intercellular adhesion molecule-1 ( ICAM-1) and vascular adhesion molecule- 1 ( VCAM- 1). Results: CSF and serum samples correlated well during nearly the whole time course ( p < 0.0001). A secondary increase in ICAM-1 and VCAM- 1 in the serum and CSF correlated with an increase in flow velocity in the transcranial Doppler ( p > 0.0001 and p < 0.007) but not to a delayed lesion in the CT scan. Conclusion: We believe that inflammatory processes are involved in the pathogenesis of cerebral vasospasm but they might only be a part of a multifactorial pathogenesis. Copyright (c) 2006 S. Karger AG, Basel