Petito C K, Schaefer J A, Plum F
Brain Res. 1977 May 27;127(2):251-67. doi: 10.1016/0006-8993(77)90539-x.
During experimental seizures, the blood-brain barrier (BBB) is broken; tracer substances such as I131-albumin, Evans blue and horseradish peroxidase (HRP) geographically locate the barrier breakdown primarily in the diencephalon. Using rats, we have induced seizures with electroshocks and demonstrated the breakdown of the BBB with Evans blue and HRP. We have shown that (1) the BBB breakdown is proportional to the number of electroconvulsant shocks (ES) given; (2) the mechanism of increased barrier permeability is primarily by micropinocytosis in the cerebral capillaries, arterioles, and, to a lesser extent, venules; and (3) the stimulus for micropinocytosis and hence BBB breakdown is associated with the abrupt rise in systemic blood pressure and cerebral vasodilatation that accompanies each ES. If the systolic hypertension is abolished via cervical cordotomy, there is little to no breakdown in the BBB.
在实验性癫痫发作期间,血脑屏障(BBB)会被破坏;诸如I131 - 白蛋白、伊文思蓝和辣根过氧化物酶(HRP)等示踪物质在地理位置上主要将屏障破坏定位在间脑。我们使用大鼠,通过电击诱发癫痫发作,并使用伊文思蓝和HRP证明了血脑屏障的破坏。我们已经表明:(1)血脑屏障的破坏与给予的惊厥电休克(ES)次数成正比;(2)屏障通透性增加的机制主要是通过脑毛细血管、小动脉,以及在较小程度上通过小静脉中的微胞饮作用;(3)微胞饮作用以及因此导致的血脑屏障破坏的刺激与每次ES伴随的全身血压突然升高和脑血管扩张有关。如果通过颈髓切断术消除收缩期高血压,则血脑屏障几乎没有破坏。