Stroke, Vol 20, 1260-1266, Copyright © 1989 by American Heart Association
T Shigeno, T Asano, T Mima and K Takakura
We hypothesize that enhanced activity of capillary Na,K-ATPase promotes Na+
influx into the brain and causes early edema formation in focal cerebral
ischemia. The pharmacologic suppression of brain capillary Na,K-ATPase as a
means to ameliorate edema formation was examined using the middle cerebral
artery occlusion model in 36 cats. With the help of a catheter inserted
into the middle cerebral artery, the ischemic brain area was directly
perfused with 10(-5) M ouabain. Perfusion was maintained as intermittent
15-second pulse injections given every 5 (n = 6) or 2 (n = 6) minutes. By
this method, the naturally occurring circulatory conditions during ischemia
were not altered. Four hours after ischemia, the cortical specific gravity
at each of six locations over the ischemic area was compared with the
corresponding ischemic blood flow measured by the H2 clearance technique.
The results show that ouabain perfused every 2 minutes significantly
ameliorated edema formation compared with six control cats perfused with
Krebs-Ringer solution. In a separate series of experiments, the Na+ flux
across the blood-brain barrier was studied by injecting 22NaCl together
with an intravascular reference (cobalt-57-labeled microspheres 15 microns
in diameter) into the ischemic area. The brain uptake index of 22Na was
markedly increased in the ischemic cortex of six control cats; ouabain
treatment in six cats suppressed the increase of Na+ influx. The results
support our hypothesis that brain capillary Na,K-ATPase activity increases
during early focal ischemia, leading to enhanced Na+ together with H2O flux
across the blood-brain barrier.
ARTICLES
Effect of enhanced capillary activity on the blood-brain barrier during focal cerebral ischemia in cats
Department of Neurosurgery, Saitama Medical School, Japan.
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1989 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |