Abstract
In order to clarify the mechanism of development of ischemic brain edema, the blood-brain barrier in Wistar rats was observed by the electron microscopic histochemical technique. In experimental models, the bilateral carotid arteries were occluded for 2hr with or without 30min exposure to nitrogen. The brains were perfused with a fixative containing 2% paraformaldehyde and 0.25% glutaraldehyde for 15min.
In controls, Mg-ATPase activity (Ogawa and Mayahara 1969) was localized on the basal surface of capillary endothelium and the astrocytic plasma membrane, and alkaline phosphatase (ALPase) (Mayahara et al. 1967) was demonstrated on both the luminal and basal plasma membranes of capillary endothelium with some variations. The reaction products of Mg-ATPase were coarsely distributed and increased in the ischemic group without nitrogen exposure. However, it markedly decreased in the anoxic-ischemic group which showed marked swelling of astrocytic foot processes. ALPase tended to be well preserved in both experimental groups, but showed focal dispersion in the anoxic-ischemic group.
The decreased activities of Mg-ATPase as well as ALPase may change the membrane permeability, and may induce intracytoplasmic fluid accumulation which causes brain edema in the early stage of ischemia.
