Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mabe, H.
Right arrow Articles by Ohno, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mabe, H.
Right arrow Articles by Ohno, M.

Stroke, Vol 17, 501-505, Copyright © 1986 by American Heart Association


ARTICLES

Effect of nimodipine on cerebral functional and metabolic recovery following ischemia in the rat brain

H Mabe, H Nagai, T Takagi, S Umemura and M Ohno

Whether the calcium entry blocker, nimodipine, prevents the increase in the concentration of free fatty acids and metabolic disturbances during ischemia and promotes functional and metabolic recovery after recirculation were examined. Severe forebrain ischemia in rats was induced by four-vessel occlusion with mild hypotension. After 30 minutes of ischemia, recirculation was started by removal of the arterial clamps and by increasing blood pressure to the preischemic level. Recovery of EEG activity following recirculation was better in the nimodipine-treated group than in the control group. During the ischemic period, there were no significant differences in accumulation of free fatty acids or in depletion of ATP between treated and control groups. At 120 minutes following recirculation, recovery of the ATP level was significantly better in the treated group than in the control group. Therefore, the promotion of functional and metabolic recovery by nimodipine-treatment is suggested to be not due to the prevention of an accumulation of free fatty acids nor to the depletion of ATP during the ischemic period, but to either improvement of postischemic hypoperfusion or a direct action on metabolic processes during reperfusion period.


This article has been cited by other articles:


Home page
StrokeHome page
J. M. Roda, F. Carceller, E. Diez-Tejedor, and C. Avendano
Reduction of Infarct Size by Intra-Arterial Nimodipine Administered at Reperfusion in a Rat Model of Partially Reversible Brain Focal Ischemia
Stroke, October 1, 1995; 26(10): 1888 - 1892.
[Abstract] [Full Text]