BLOOD BRAIN BARRIER
Cerebral blood vessels are unique in that the junc-tions between vascular endothelial cells are nearly fused. The paucity of pores is responsible for what is termed the blood–brain barrier. This lipid barrier allows the passage of lipid-soluble substances, but restricts the movement of those that are ionized or have large molecular weights. Thus, the move-ment of a given substance across the blood brain barrier is governed simultaneously by its size, charge, lipid solubility, and degree of protein bind-ing in blood. Carbon dioxide, oxygen, and lipid-soluble molecules (such as most anesthetics) freely enter the brain, whereas most ions, proteins, and large substances (such as mannitol) penetrate poorly.
Water moves freely across the blood–brain bar-rier as a consequence of bulk flow, whereas move-ment of even small ions is impeded (the equilibration half-life of Na + is 2–4 h). As a result, rapid changes in plasma electrolyte concentrations (and, secondarily, osmolality) produce a transient osmotic gradient between plasma and the brain. Acute hypertonicity of plasma results in net movement of water out of the brain, whereas acute hypotonicity causes a net movement of water into the brain. These effects are short-lived, as equilibration eventually occurs, but, when marked, they can cause rapid fluid shifts in the brain. Mannitol, an osmotically active substance that does not normally cross the blood–brain barrier, causes a sustained decrease in brain water content and is often used to decrease brain volume.
The blood–brain barrier may be disrupted by severe hypertension, tumors, trauma, strokes,infection, marked hypercapnia, hypoxia, and sus-tained seizure activity. Under these conditions, fluid movement across the blood–brain barrier becomes dependent on hydrostatic pressure rather than osmotic gradients.
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