Vasogenic edema in terms of blood-brain barrier

用原代培养的大鼠脑毛细血管内皮细胞(RBEC)建立血脑屏障(BBB)模型，观察匹伐他汀对BBB屏障功能的影响。在10-8M浓度下，匹伐他汀可增加内皮细胞间紧密连接(TJ)屏障严密性的指标--跨内皮细胞电阻(TEER)，并降低内皮细胞对荧光素钠的通透性。在异戊二烯类香叶基焦磷酸存在下，TEER的增加显著减少，而法尼基焦磷酸对TEER没有影响。我们的免疫细胞化学和Western印迹分析表明，匹伐他汀处理后，TJs的主要功能蛋白claudin-5的表达增强。我们的数据表明，匹伐他汀增强了原代培养的rBEC的屏障完整性。匹伐他汀的BBB稳定作用可能部分是通过抑制甲氧戊酸途径和随后上调claudin-5的表达来实现的。在10年的时间里，长崎大学医院收治了5例创伤性CCF患者(3男2女，年龄17-68岁)。由于引流到眼上静脉，表现为眼部症状，1例皮质反流发展为颅内出血。所有病例均行血管内弹簧圈栓塞术(动静脉分流术3例，载瘤动脉闭塞术2例)。

We investigated the effect of pitavastatin on barrier functions of an in vitro blood-brain barrier (BBB) model with primary cultures of rat brain capillary endothelial cells (RBEC). Pitavastatin increased the transendothelial electrical resistance (TEER), an index of barrier tightness of interendothelial tight junctions (TJs), at a concentration of 10-8 M, and decreased the endothelial permeability for sodium fluorescein through the RBEC monolayer. The increase in TEER was significantly reduced in the presence of isoprenoid geranylgeranyl pyrophosphate, whereas farnesyl pyrophosphate had no effect on TEER. Our immunocytochemical and Western blot analyses revealed that treatment with pitavastatin enhanced the expression of claudin-5, a main functional protein of TJs. Our data indicate that pitavastatin strengthens the barrier integrity in primary cultures of RBEC. The BBB-stabilizing effect of pitavastatin may be mediated partly through inhibition of the mevalonate pathway and subsequent up-regulation of claudin-5 expression.During a 10-year period, five cases (three men and two women, 17-68 years) of traumatic CCF were treated at the Nagasaki University hospital. They represented ophthalmic symptoms because of drainage to the superior ophthalmic vein, and one case with cortical reflux developed intracranial hemorrhage. All cases were managed with endovascular coil embolization (three arteriovenous shunt occlusion, two parent artery occlusion).