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Blood-Brain Barrier

In most of the body's capillary beds, fenestrations approximately 65 Å in diameter are found between endothelial cells. In the brain, with the exception of the choroid plexus, the pituitary, and the area postrema, tight junctions reduce this pore size to approximately 8 Å. As a result, large molecules and most ions are prevented from entering the brain's interstitium. There is little evidence that anesthetics alter the function of this "blood-brain barrier" in most circumstances. However, it has repeatedly been demonstrated that acute hypertension can breath the barrier[402] [403] [404] and that certain anesthetics facilitate this phenomenon.[405] Forster and colleagues[406] observed that extravasation of Evans blue into rabbit brain was greater when acute hypertension occurred during anesthesia with halothane than with thiopental. It is probable that this effect is the nonspecific result of cerebral vasodilation[407] rather than a specific effect of halothane. These results were obtained in the setting of extreme, abrupt hypertension in animals with an initially normal BBB. Evidence also indicates that anesthetics may influence the leakiness of an abnormal BBB at normotension. Smith and Marque[408] subjected dogs to 5 hours of anesthesia after a freeze lesion (which causes an opening in the BBB). Accumulation of


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cerebral water at 24 hours was less in animals anesthetized with pentobarbital or fentanyl-droperidol-N2 O than with halothane, enflurane, or isoflurane. To our knowledge, no peer-reviewed investigation has attempted a comparison of the effects of anesthetics on BBB function during anesthesia in normotensive humans.

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