Characterization of microvascular basal lamina damage and blood-brain barrier dysfunction following subarachnoid hemorrhage in rats
Characterization of microvascular basal lamina damage and blood-brain barrier dysfunction following subarachnoid hemorrhage in rats
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DOI：
10.1016/j.brainres.2007.01.034
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发表时间：
2007-04-20
期刊：
影响因子：
2.9
通讯作者：
Zausinger, Stefan
中科院分区：
文献类型：
--
作者：
Schoeller, Karsten;Trinkl, Andreas;Zausinger, Stefan
血管源性脑水肿是蛛网膜下腔出血(SAH)后死亡率的主要决定因素之一。尽管血管源性脑水肿的形成是通过内皮紧密连接的开放和基底板的破坏在微血管水平上发生的，但实验性蛛网膜下腔出血后微血管的变化特征尚不清楚。因此，本研究的目的是探讨SAH后血脑屏障(BBB)功能障碍和基底膜损伤的时间进程，为更好地了解SAH的病理生理学奠定基础。用血管内细丝诱导SD大鼠SAH。分别于术后6、24、48、72h处死动物，每组9只。用IV型胶原免疫组织化学染色检测微血管基底板的损伤程度。Western blotting定量IV型胶原蛋白含量和牛血清白蛋白(BSA)渗出量，分别作为基底膜损伤和血脑屏障破坏的指标。BSA Western印迹显示显著(p
Vasogenic brain edema is one of the major determinants for mortality following subarachnoid hemorrhage (SAH). Although the formation of vasogenic brain edema occurs on the microvascular level by opening of endothelial tight junctions and disruption of the basal lamina, microvascular changes following experimental SAH are poorly characterized. The aim of the present study was therefore to investigate the time course of blood-brain barrier (BBB) dysfunction and basal lamina damage following SAH as a basis for the better understanding of the pathophysiology of SAH. SAH was induced in Sprague-Dawley rats by an endovascular filament. Animals were sacrificed 6, 24, 48, and 72 h thereafter (n=9 per group). Microvascular basal lamina damage was quantified by collagen type IV immunostaining. Western blotting was used to quantify collagen IV protein content and bovine serum albumin (BSA) extravasation as a measure for basal lamina damage and blood-brain barrier disruption, respectively. BSA Western blot revealed significant (p