Stroke, Vol 22, 495-498, Copyright © 1991 by American Heart Association
TN Lin, TH Liu, J Xu, CY Hsu and GY Sun
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.
ARTICLES
Brain polyphosphoinositide metabolism during focal ischemia in rat cortex
Biochemistry Department, University of Missouri, Columbia 65212.
This article has been cited by other articles:
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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] |
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