Causes of disruption of bloodbrain barrier function

Infection Inflammation Neoplastic infiltration Circulating toxins

Cerebral ischaemia and reperfusion Malignant hypertension Osmotic injury Seizure activity molecular weight for allowing free diffusion is below 400-600 daltons. Pinocytotic vesicles transport plasma and interstitial fluid bidirectionally across the endothelium. The capillary endothelial cells have a high mitochondrial content to supply energy for the transport of water-soluble substances. P-glycoprotein, a unique membrane glycoprotein with a molecular weight of 170-180 kDa, is expressed at the luminal membrane of the endothelial cells and at the astrocytic foot processes.

The blood-brain barrier can be bypassed by intrathecal administration of drugs into the CSF and by drug modification (increased lipid solubility; carrier transport). Disruption of barrier function can be recognised radiologically on computed tomographic scanning by the phenomenon of contrast enhancement, and is associated with vasogenic cerebral oedema. Disruption is associated with acute increases in CSF protein levels. Loss of integrity of the barrier function is related to partial and reversible relaxation of endothelial tight junctions, and to increased vesicular transport across the endothelial cells.

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