Handa Y, Kubota T, Kaneko M, Tsuchida A, Kobayashi H, Kawano H, Kubota T
Department of Neurosurgery, Fukui Medical School, Japan.
Acta Neurochir (Wien). 1995;132(1-3):92-7. doi: 10.1007/BF01404854.
In order to study how immune-inflammatory responses are involved in the pathogenesis of cerebral vasospasm after subarachnoid haemorrhage (SAH), the kinetics of expression of the intercellular adhesion molecule 1 (ICAM-1), a ligand for the leucocyte adhesion receptor, were studied on the cerebral arteries following SAH in rats. The SAH was induced by intracisternal injection of arterial blood. The rats were sacrificed at specified times: immediately after induction of SAH to seven days after SAH. Cryostat sections of the basilar artery (BA) were prepared and incubated with anti-rat ICAM-1 antibody. Morphometric analysis of the BA revealed a significant narrowing of the luminal diameter on Day 2 following SAH. While in the non-treated normal animals, no nor only weak expression of ICAM-1 was observed on the endothelial layer of the BA, there was greater expression of ICAM-1 on the endothelial layer of the BA in SAH rats, and the expression was observed also in the medial layer of the artery from Day 2 to Day 5 following SAH. The present results indicate that SAH really causes responses in the cellular immunity not only in the endothelial layer, but also in the medial layer of the artery as a target of immune damage, which is presumed to be one of the important steps in the development of cerebral vasospasm.
为了研究免疫炎症反应如何参与蛛网膜下腔出血(SAH)后脑血管痉挛的发病机制,我们对大鼠SAH后大脑动脉中白细胞粘附受体的配体细胞间粘附分子1(ICAM-1)的表达动力学进行了研究。通过脑池内注射动脉血诱导SAH。在特定时间处死大鼠:SAH诱导后立即至SAH后七天。制备基底动脉(BA)的低温切片,并用抗大鼠ICAM-1抗体孵育。对BA的形态学分析显示,SAH后第2天管腔直径显著变窄。在未处理的正常动物中,BA内皮细胞层未观察到或仅观察到弱的ICAM-1表达,而在SAH大鼠的BA内皮细胞层有更强的ICAM-1表达,并且在SAH后第2天至第5天在动脉中层也观察到表达。目前的结果表明,SAH不仅在内皮层,而且在作为免疫损伤靶点的动脉中层确实引起细胞免疫反应,这被认为是脑血管痉挛发展的重要步骤之一。