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 Lin, T. N.
Right arrow Articles by Sun, G. Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lin, T. N.
Right arrow Articles by Sun, G. Y.

Stroke, Vol 22, 495-498, Copyright © 1991 by American Heart Association


ARTICLES

Brain polyphosphoinositide metabolism during focal ischemia in rat cortex

TN Lin, TH Liu, J Xu, CY Hsu and GY Sun
Biochemistry Department, University of Missouri, Columbia 65212.

Using a rat model of stroke, we examined the effects of focal cerebral ischemia on the metabolism of polyphosphoinositides by injecting 32Pi into both the left and right cortices. After equilibration of the label for 2-3 hours, ischemia induced a significant decrease (p less than 0.001) in the concentrations of labeled phosphatidyl 4,5-bisphosphates (66-78%) and phosphatidylinositol 4-phosphate (64-67%) in the right middle cerebral artery cortex of four rats. The phospholipid labeling pattern in the left middle cerebral artery cortex, which sustained only mild ischemia and no permanent tissue damage, was not different from that of two sham-operated controls. However, when 32Pi was injected 1 hour after the ischemic insult, there was a significant decrease (p less than 0.01) in the incorporation of label into the phospholipids in both cortices of four ischemic rats compared with four sham-operated controls. Furthermore, differences in the phospholipid labeling pattern were observed in the left cortex compared with the sham-operated controls. The change in labeling pattern was attributed to the partial reduction in blood flow following ligation of the common carotid arteries. We provide a sensitive procedure for probing the effects of focal cerebral ischemia on the polyphosphoinositide signaling pathway in the brain, which may play an important role in the pathogenesis of tissue injury.


This article has been cited by other articles:


Home page
StrokeHome page
G.Y. Sun, J.-P. Zhang, T.A. Lin, T.-N. Lin, Y.Y. He, and C.Y. Hsu
Inositol Trisphosphate, Polyphosphoinositide Turnover, and High-Energy Metabolites in Focal Cerebral Ischemia and Reperfusion
Stroke, October 1, 1995; 26(10): 1893 - 1900.
[Abstract] [Full Text]