Abstract
Intravenous administration of Clostridium perfringens type D episilon toxin to mice causes severe, generalized, vascular endothelial damage and progressive brain oedema. The brain oedema is revealed as a quantitive increase in the water content of brain tissue and a swelling of protoplasmic astrocytes and astrocytic processes around blood vessels and in the neuropil.
The use of horse radish peroxidase as a tracer has indicated that the endothelial damage may also allow proteins to escape from the vascular lumen into the extracellular spaces of the brain.
The suitability of Cl. perfringens type D epsilon toxin intoxication as a model for studying brain oedema and related problems is discussed.
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