Raymond J J, Robertson D M, Dinsdale H B
Can J Neurol Sci. 1986 Aug;13(3):214-20. doi: 10.1017/s0317167100036301.
Internal carotid artery infusion of bradykinin caused extensive breakdown of the blood-brain barrier to protein as demonstrated by the extravasation of the marker, horseradish peroxidase, into vessel walls and the adjacent parenchyma. Pretreatment of the animals with indomethacin, trifluoperazine, or imidazole significantly reduced the quantity of abnormally permeable vessels as determined by light microscopy. By electron microscopy, it was determined that bradykinin caused an intense increase in the number of pinocytotic vesicles in the permeable segments, but no change in the interendothelial junctions. After imidazole pretreatment, although the extent of the permeability change was markedly reduced, the intensity of pinocytotic activity in the involved areas was not altered.
向颈内动脉注入缓激肽会导致血脑屏障对蛋白质的广泛破坏,这可通过标记物辣根过氧化物酶渗入血管壁和邻近实质来证明。用吲哚美辛、三氟拉嗪或咪唑对动物进行预处理,通过光学显微镜观察发现,异常通透性血管的数量显著减少。通过电子显微镜观察发现,缓激肽会使通透性节段内吞小泡的数量急剧增加,但内皮细胞间连接并无变化。咪唑预处理后,虽然通透性变化的程度明显降低,但受累区域内吞活性的强度并未改变。