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|Title:||Toxin-induced vasogenic cerebral oedema in a rat model|
|Citation:||Brain edema XI : proceedings of the 11th International Symposium, 6-10 June, 1999 / A.D. Mendelow [et al.] (eds.): pp.231-236|
|Series/Report no.:||Acta neurochirurgica. Supplement no. 76|
|Conference Name:||International Symposium on Brain Edema (11th : 1999 : Newcastle upon Tyne, England)|
|Mounir N Ghabriel, C Zhu, PL Reilly, PC Blumbergs, J Manavis, JW Finnie|
|Abstract:||Vasogenic cerebral oedema (VCO) was induced in Hooded Wistar rats by intraperitoneal injection of Clostridium perfringens type D epsilon prototoxin. Animals were killed, 1 h to 14 d postinjection, by perfusion fixation under general anaesthesia. VCO was detected by the presence of endogenous albumin in the brain, visualised by immunocytochemistry. As early as 1 h postinjection, albumin was detected in the walls of cerebral microvessels. Maximal diffuse leakage within the neural parenchyma was seen at 24 and 48 h and immunoreactivity was still present at 4 d. At 7 d only few foci were seen, and at 14 d albumin distribution was similar to that in controls. Ultrastructural assessment of the microvessels showed swelling of many astrocytic processes and abnormalities of the endothelial cells varying from swelling with loss of cytoplasmic organelles to cells showing increased electron density. Immunostaining for the endothelial barrier antigen (EBA) showed strongly immunoreactive vessels throughout normal brains. Experimental animals showed partial reduction in EBA expression, most evident at 24 and 48 h, with gradual recovery to normal by 14 d. The exact role that EBA plays in the intact BBB remains obscure.|
Disease Models, Animal
|Description:||The original publication can be found at www.springerlink.com|
|Appears in Collections:||Anatomical Sciences publications|
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