Stroke, Vol 23, 1331-1336, Copyright © 1992 by American Heart Association
GY Yang, SF Chen, H Kinouchi, PH Chan and PR Weinstein
BACKGROUND AND PURPOSE: Reduction of cerebral blood flow results in several
acute metabolic disturbances, including a reduction in Na,K- ATPase
activity. The relation between this reduction and the onset of edema is
unknown, as is the effect of restoration of blood flow. Therefore, we
investigated the role of decreased Na,K-ATPase activity in the pathogenesis
and time course of ischemic brain edema and reperfusion. METHODS: The
middle cerebral arteries of rats were occluded by cannulation with a nylon
suture for 30, 60, 120, or 240 minutes. The animals were then decapitated
(permanent occlusion) or the suture was withdrawn to allow 24 hours of
reperfusion before decapitation (temporary occlusion). Na,K-ATPase activity
and Na+, K+ and water contents were measured at various intervals. RESULTS:
In the ischemic hemisphere, Na,K-ATPase activity was significantly
decreased at 30, 60, 120, and 240 minutes of permanent occlusion (p less
than 0.05). There was also a significant decrease in rats subjected to 60
or 120 minutes of temporary occlusion followed by 24 hours of reperfusion.
Water content increased after 60, 120, or 240 minutes of permanent
occlusion (p less than 0.01); after 24 hours of reperfusion, water content
remained elevated (p less than 0.01). The Na+ content increased after both
permanent and temporary occlusion, and the K+ content decreased only after
permanent occlusion. Increases in water content correlated with decreases
in Na,K-ATPase activity after temporary occlusion and with the Na+:K+ ratio
after permanent occlusion. CONCLUSION: Reduction in Na,K-ATPase activity
resulting in disruption of cellular ionic homeostasis may account for early
development of cytotoxic brain edema after permanent occlusion of the
middle cerebral artery. Such edema is also present 24 hours after 60 and
120 but not 30 minutes of temporary occlusion.
ARTICLES
Edema, cation content, and ATPase activity after middle cerebral artery occlusion in rats
Department of Neurological Surgery, School of Medicine, University of California, San Francisco.
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