Stroke, Vol 19, 1275-1282, Copyright © 1988 by American Heart Association
M Seida, HG Wagner, K Vass and I Klatzo
We attempted to ameliorate postischemic edema and brain tissue injury in
cats by administering aminophylline to reduce the reactive hyperemia that
supposedly aggravates both these sequelae. Forty-one cats were subjected to
1 hour of middle cerebral artery occlusion and were killed after 3 hours, 3
days, or 14 days of recirculation; one half of the cats received 0.916
ml/kg of a 25 mg/ml solution of aminophylline by infusion at a constant
rate via the femoral vein starting 10 minutes before release of the
occlusion and continuing for 5 minutes after initiation of recirculation;
the other half received saline. Regional cerebral blood flow was monitored
by the hydrogen clearance method and water content was evaluated by
specific gravity measurements after 3 hours of recirculation; the status of
the blood-brain barrier was assessed with Evans blue tracer. Morphologic
observations were carried out in cats killed after 3 or 14 days of
recirculation. Aminophylline- treated cats killed after 3 hours of
recirculation showed significantly reduced hyperemia and edema and no
leakage of Evans blue, which was present in all untreated cats killed after
3 hours or 3 days of recirculation. Morphologic observations revealed
conspicuously more severe ischemic brain tissue damage in the untreated
than in the aminophylline-treated cats after 3 and 14 days of
recirculation. Our studies indicate the beneficial effect of administration
of aminophylline in the amelioration of postischemic edema and brain tissue
injury, which is presumably achieved by reduction of reactive hyperemia.
ARTICLES
Effect of aminophylline on postischemic edema and brain damage in cats
Laboratory of Neuropathology and Neuroanatomical Sciences, National Institute of Neurological and Communicative Disorders and Stroke, Bethesda, MD 20892.
This article has been cited by other articles:
![]() |
T. W. Hein, Z. Yuan, R. H. Rosa Jr, and L. Kuo Requisite Roles of A2A Receptors, Nitric Oxide, and KATP Channels in Retinal Arteriolar Dilation in Response to Adenosine Invest. Ophthalmol. Vis. Sci., June 1, 2005; 46(6): 2113 - 2119. [Abstract] [Full Text] [PDF] |
||||
|
Stroke Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1988 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |