Donate Help Contact The AHA Sign In Home
American Heart Association
Stroke
Search: search_blue_button Advanced Search
Stroke. 1989;20:1524-1530

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 arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Scremin, O. U.
Right arrow Articles by Jenden, D. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scremin, O. U.
Right arrow Articles by Jenden, D. J.

Stroke, Vol 20, 1524-1530, Copyright © 1989 by American Heart Association


ARTICLES

Effects of middle cerebral artery occlusion on cerebral cortex choline and acetylcholine in rats

OU Scremin and DJ Jenden
Veterans Administration Medical Center, Albuquerque, New Mexico 87108.

We measured regional cerebral blood flow and acetylcholine and choline concentrations in tissue fragments of normally perfused and ischemic cortical regions from 10 rats. Tissue uptake of [14C]iodoantipyrine was used to indicate regional cerebral blood flow, and gas chromatography- mass spectrometry was used to measure acetylcholine and choline concentrations. Cerebral cortical ischemia was induced by permanent occlusion of the middle cerebral artery, and variables were measured 2.5 or 24 hours later. A close correlation was found between tissue choline concentration and the reciprocal of regional cerebral blood flow. A large increase in tissue choline concentration was observed in the ischemic cortex. Choline production rate was estimated by plotting choline concentration against the reciprocal of regional cerebral blood flow. This rate was independent of choline concentration. Acetylcholine concentration, on the other hand, was constant in ischemic and normally perfused regions, except in the center of the ischemic region 2.5 hours after middle cerebral artery occlusion, where a significant decrease was observed.


This article has been cited by other articles:


Home page
J. Biol. Chem.Home page
N. Takagi, K. Miyake-Takagi, K. Takagi, H. Tamura, and S. Takeo
Altered Extracellular Signal-regulated Kinase Signal Transduction by the Muscarinic Acetylcholine and Metabotropic Glutamate Receptors after Cerebral Ischemia
J. Biol. Chem., February 15, 2002; 277(8): 6382 - 6390.
[Abstract] [Full Text] [PDF]


Home page
StrokeHome page
D. E. Saunders, F. A. Howe, A. van den Boogaart, M. A. McLean, J. R. Griffiths, and M. M. Brown
Continuing Ischemic Damage After Acute Middle Cerebral Artery Infarction in Humans Demonstrated by Short-Echo Proton Spectroscopy
Stroke, June 1, 1995; 26(6): 1007 - 1013.
[Abstract] [Full Text]