Abstract
Mechanisms of early cerebral edema following SAH are poorly understood. Previously, we demonstrated a peak of edema evolution at 24 hours after experimental SAH in rats. Furthermore, brain water content correlated with neurological deficits of animals. In focal cerebral ischemia, alteration of the microvascular basal lamina, a constituent of the blood-brain barrier, and its relevance for development of cerebral edema and hemorrhagic transformation has previously been demonstrated. The present study was designed to demonstrate microvascular basal lamina damage in the context of blood-brain barrier dysfunction as a potential target for therapeutical interventions to reduce vasogenic brain edema following SAH.
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