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Vol. 289, Issue 2, 668-675, May 1999
Department of Pharmacology, University of Arizona College of
Medicine, Tucson, Arizona
Increased cerebrovascular permeability is an important factor in the
development of cerebral edema after stroke, implicating the blood-brain
barrier (BBB) in the pathology of stroke. Present investigations
modeled stroke at the level of the cerebral capillary endothelium by
analyzing BBB permeability changes to the membrane-impermeant marker
[14C]sucrose after hypoxia/aglycemia. Under hypoxia
alone, long exposures (48 h) were necessary to result in a significant
increase in permeability of bovine brain microvessel endothelial cells
to [14C]sucrose. Hypoxia/aglycemia exposures resulted in
a much shorter time (i.e., 1-3 h) required for a corresponding
increase in permeability to [14C]sucrose. Statistically
significant changes in basal permeability were observed between 3 and
6 h of hypoxia/aglycemia; however, 6 h of aglycemia alone had
no significant effect on BBB permeability. Both rat astroglioma (C6)
cells and C6 conditioned medium showed no improvements in barrier
function measured by transendothelial cell resistance or permeability
to [14C]sucrose. Changes in endothelial cell calcium flux
may be responsible for the permeability change observed after both
48 h of hypoxia and 6 h of hypoxia/aglycemia because
nifedipine (10 and 100 nM) and SKF 96365 (100 nM) decreased the
permeability change. Immunocytochemical studies also revealed a change
in the distribution of endothelial cell F-actin. This study provides
evidence that the BBB is sensitive to short exposures of
hypoxia/aglycemia and that changes in endothelial cell calcium flux may
be responsible for structural and functional variations in the BBB
during ischemic stress.
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