Stroke, Vol 18, 1157-1159, Copyright © 1987 by American Heart Association
M Watanabe and WI Rosenblum
We studied pial vessels in vivo in mice, examining under mercury light the
permeability of these vessels to sodium fluorescein. Topical application of
hypertonic solutions of NaCl caused leakage of fluorescein. However,
putative chemical mediators of leakage, such as histamine, serotonin,
arachidonic acid, and bradykinin, all failed to increase permeability to
the dye. Apparent increases in permeability only accompanied endothelial
damage caused by the dye + light combination, as indicated by production of
local platelet aggregates. The technique is useful, provided inadvertent
endothelial injury is recognized and avoided. The data in mice suggest that
pial vessels may not participate in the permeability changes reportedly
produced in parenchymal brain vessels by several of the mediators we
tested. Therefore, studies of pial vascular permeability are not expected
to provide reliable data concerning the actions of agents that might
mediate cerebral edema.
ARTICLES
In vivo studies of pial vascular permeability to sodium fluorescein: absence of alterations by bradykinin, histamine, serotonin, or arachidonic acid
Department of Pathology (Neuropathology), Medical College of Virginia, Virginia Commonwealth University, Richmond, Va. 23298.
This article has been cited by other articles:
![]() |
A. F. Heck Permeability of Intracranial Blood Vessels to Endogenous Serum Albumin Angiology, March 1, 1990; 41(3): 233 - 240. [Abstract] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1987 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |