Vorbrodt A W, Dobrogowska D H, Lossinsky A S
New York State Office of Mental Retardation and Developmental Disabilities, Institute for Basic Research in Developmental Disabilities, Staten Island 10314, USA.
J Neurocytol. 1996 Nov;25(11):645-57. doi: 10.1007/BF02284831.
The main objective of this ultrastructural study was to gain insights into the cellular mechanisms responsible for the enhanced brain uptake of blood-borne cationized albumin observed by several authors utilizing quantitative methodology. Mice were injected intravenously or into the common carotid artery (in vivo experiments) or perfused in situ with solutions of native or cationized bovine serum albumin complexed with colloidal gold (BSA-G or cBSA-G respectively). The results indicate that: (1) the main drawbacks of in vivo experiments are very intense phagocytosis of the tracer particles by Kupffer cells located in the liver sinusoids and also escape of the tracer through capillaries of skeletal and heart muscles. This results in a rapid decline of the concentration and disappearance of the circulating tracer particles; (2) BSA-G and cBSA-G both in vivo (up to 30 min circulation) or after perfusion in situ (up to 15 min) do not cross the wall of brain microvessels representing the blood-brain barrier; (3) enhanced entrance of cationized albumin into the brain occurs through fenestrated endothelium of the capillaries located in the examined circumventricular organs (median eminence and neurohypophysis). Although BSA-G is also transported by these fenestrated capillaries, this process is evidently less intense than in the case of cBSA-G; (4) the enhanced passage of cBSA-G across fenestrated capillaries occurs mainly via vesicular transport (adsorptive transcytosis), through transendothelial channels and eventually through interendothelial junctional clefts; (5) the fenestrated capillaries of the choroid plexus appear to be less permeable for both tracers than those located in the other circumventricular organs.
这项超微结构研究的主要目的是深入了解细胞机制，这些机制是几位作者利用定量方法观察到的血源性阳离子化白蛋白脑摄取增强的原因。给小鼠静脉注射或注入颈总动脉（体内实验），或用与胶体金复合的天然或阳离子化牛血清白蛋白溶液（分别为BSA-G或cBSA-G）进行原位灌注。结果表明：（1）体内实验的主要缺点是位于肝血窦的库普弗细胞对示踪颗粒的吞噬作用非常强烈，并且示踪剂会通过骨骼肌和心肌的毛细血管逸出。这导致循环示踪颗粒的浓度迅速下降并消失；（2）无论是在体内（循环长达30分钟）还是原位灌注后（长达15分钟），BSA-G和cBSA-G都不会穿过代表血脑屏障的脑微血管壁；（3）阳离子化白蛋白进入脑的增强是通过位于所检查的室周器官（正中隆起和神经垂体）的有窗内皮实现的。虽然BSA-G也由这些有窗毛细血管运输，但这个过程显然不如cBSA-G的情况强烈；（4）cBSA-G穿过有窗毛细血管的增强主要通过囊泡运输（吸附转胞吞作用）、通过跨内皮通道并最终通过内皮间连接缝隙；（5）脉络丛的有窗毛细血管对两种示踪剂的通透性似乎比其他室周器官中的有窗毛细血管低。
