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 arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kempski, O.
Right arrow Articles by Feuerstein, G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kempski, O.
Right arrow Articles by Feuerstein, G.

Stroke, Vol 18, 111-119, Copyright © 1987 by American Heart Association


ARTICLES

Postischemic production of eicosanoids in gerbil brain

O Kempski, E Shohami, D von Lubitz, JM Hallenbeck and G Feuerstein

The postischemic production of PGE2, PGD2, 6-keto-PGF1 alpha, and TXB2 in brain tissue was studied in Mongolian gerbils using tissue extraction as well as a new ex vivo method. This new method permits the study of prostaglandin synthesis in slices from discrete areas of the brain (cortex, hippocampus, striatum, hypothalamus). Gerbils were sacrificed at 0, 5, and 30 minutes, and 4 and 24 hours after a 15- minute occlusion of both carotid arteries. Apart from 6-keto-PGF1 alpha, tissue prostaglandins determined by the extraction method were significantly increased 3 and 30 minutes after reperfusion. The most pronounced changes found by the ex vivo method were increased productions of PGD2 immediately after reperfusion (285% in cortex, 215% in hypothalamus) and PGE2 (350% in hippocampus, 320% in striatum) 4 hours after reperfusion. At 24 hours after reperfusion PGE2 and PGD2 synthesis were significantly decreased by 23-70% of the values obtained from sham-operated controls. Thromboxane increased slightly in all areas after recirculation and subsequently decreased to values below the control level in striatum. The results obtained by ex vivo incubation of tissue slices demonstrate that ischemia and subsequent recirculation cause site-, time-, and PG-specific changes of tissue eicosanoid production.


This article has been cited by other articles:


Home page
Proc. Natl. Acad. Sci. USAHome page
Y. Ikeda-Matsuo, A. Ota, T. Fukada, S. Uematsu, S. Akira, and Y. Sasaki
Microsomal prostaglandin E synthase-1 is a critical factor of stroke-reperfusion injury
PNAS, August 1, 2006; 103(31): 11790 - 11795.
[Abstract] [Full Text] [PDF]


Home page
StrokeHome page
J. A. Clemens, D. T. Stephenson, E. B. Smalstig, E. F. Roberts, E. M. Johnstone, J. D. Sharp, S. P. Little, and R. M. Kramer
Reactive Glia Express Cytosolic Phospholipase A2 After Transient Global Forebrain Ischemia in the Rat
Stroke, March 1, 1996; 27(3): 527 - 535.
[Abstract] [Full Text]


Home page
StrokeHome page
W. Stummer, A. Baethmann, R. Murr, L. Schurer, and O. S. Kempski
Cerebral Protection Against Ischemia by Locomotor Activity in Gerbils : Underlying Mechanisms
Stroke, August 1, 1995; 26(8): 1423 - 1430.
[Abstract] [Full Text]