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
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.