Rapoport S I, Matthews K, Thompson H K, Pettigrew K D
Brain Res. 1977 Nov 4;136(1):23-9. doi: 10.1016/0006-8993(77)90128-7.
The blood-brain barrier in the rhesus monkey was opened to intravascular Evans blue-albumin, without causing brain edema or altering brain electrolytes, by perfusing 2.5 molal recrystallized D,L-lactamide into the internal carotid artery for 20--30 sec. Gross neurological and behavioral sequelae were absent in 7 of 8 animals with barrier opening, and 2 days after perfusion no statistically significant changes were observed in sodium, potassium or water contents of perfused as compared to unperfused gray and white matters of brains of the 7 normal animals. Brain endema may not have developed because parenchymal albumin was excreted or metabolized by 2 days. It is suggested also that closure of the barrier after several hours prevents salt from accompanying plasma fluid into the brain. Entry of fluid without salt would reduce, before measurable edema developed, any transcapillary osmotic gradient established by prior entry of plasma albumin.
通过向恒河猴的颈内动脉灌注2.5摩尔重结晶的D，L-乳酰胺20 - 30秒，使恒河猴的血脑屏障对血管内伊文思蓝-白蛋白开放，而不引起脑水肿或改变脑电解质。8只进行屏障开放的动物中有7只没有明显的神经和行为后遗症，灌注后2天，与7只正常动物未灌注的脑灰质和白质相比，灌注的脑灰质和白质中的钠、钾或水分含量没有观察到统计学上的显著变化。脑水肿可能没有发生，因为2天时实质白蛋白已被排泄或代谢。还表明，数小时后屏障的关闭可防止盐分随血浆液体进入大脑。在可测量的水肿出现之前，无盐液体的进入会减少由先前血浆白蛋白进入所建立的任何跨毛细血管渗透梯度。
