Linked Life Data

16567054

Source:http://linkedlifedata.com/resource/pubmed/id/16567054

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-5-22
pubmed:abstractText
We examined the role of cyclooxygenase-2 in the development of ischemic tolerance induced by cortical spreading depression against transient, focal brain ischemia. Cortical spreading depression was continuously induced for 2 h with topical KCl (13+/-1 depolarizations/2 h) in male Wistar rats. At 1, 2, 3, 4, and 5 days following recovery, the middle cerebral artery was transiently occluded for 120 min. Four days later, the animals were killed and infarct volume was determined. Additionally, cyclooxygenase-2 levels in the cerebral cortex and 15 deoxy-Delta(12, 14) PGJ2 levels in cerebrospinal fluid were determined at these times with Western blotting and immunoassay, respectively. Infarct volume was reduced compared with non-cortical spreading depression control animals (274.3+/-15.3 mm3) when cortical spreading depression was performed 3 and 4 days before middle cerebral artery occlusion (163.9+/-14.2 mm3, 154.9+/-14.2 mm3) but not at 1, 2 and 5 days (280.4+/-17.3 mm3, 276.3+/-16.9 mm3 and 268.5+/-17.3 mm3). Cyclooxygenase-2 levels increased most dramatically starting at 2 days, peaked at 3 days, and started to return toward baseline at 4 days after cortical spreading depression. 15 Deoxy-Delta(12, 14) PGJ2 levels increased from 134.7+/-83 pg/ml at baseline to 718+/-98 pg/ml at 3 days. Administration of N-[2-cyclohexyloxy-4-nitrophenyl] methanesulphonamide (10 mg/kg, i.v.), a selective cyclooxygenase-2 inhibitor, at 1 h prior to middle cerebral artery occlusion in cortical spreading depression preconditioned animals did not affect infarct volume (162.6+/-62.1 mm3). However, administration of N-[2-cyclohexyloxy-4-nitrophenyl] methanesulphonamide given three times prior to middle cerebral artery occlusion prevented the reduced infarct volume induced by cortical spreading depression preconditioning (272.9+/-63.2 mm3). Administration of L-nitro-arginine methyl ester (4 mg/kg, i.v.) prior to cortical spreading depression blocked increases in cyclooxygenase-2 normally seen at 3 and 4 days. We conclude that NO-mediated cyclooxygenase-2 upregulation by cortical spreading depression protects the brain against ischemic damage.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
723-30
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:16567054-Animals, pubmed-meshheading:16567054-Cerebral Cortex, pubmed-meshheading:16567054-Cerebral Infarction, pubmed-meshheading:16567054-Cortical Spreading Depression, pubmed-meshheading:16567054-Cyclooxygenase 2, pubmed-meshheading:16567054-Cyclooxygenase 2 Inhibitors, pubmed-meshheading:16567054-Cytoprotection, pubmed-meshheading:16567054-Disease Models, Animal, pubmed-meshheading:16567054-Infarction, Middle Cerebral Artery, pubmed-meshheading:16567054-Ischemic Attack, Transient, pubmed-meshheading:16567054-Ischemic Preconditioning, pubmed-meshheading:16567054-Male, pubmed-meshheading:16567054-NG-Nitroarginine Methyl Ester, pubmed-meshheading:16567054-Nitric Oxide, pubmed-meshheading:16567054-Nitric Oxide Synthase, pubmed-meshheading:16567054-Potassium Chloride, pubmed-meshheading:16567054-Prostaglandin D2, pubmed-meshheading:16567054-Rats, pubmed-meshheading:16567054-Rats, Wistar, pubmed-meshheading:16567054-Up-Regulation
pubmed:year
2006
pubmed:articleTitle
Cyclooxygenase-2 mediates the development of cortical spreading depression-induced tolerance to transient focal cerebral ischemia in rats.
pubmed:affiliation
Department of Physiology and Pharmacology, Wake Forest University Health Sciences, USA, and Department of Neurosurgery, National Hospital Organization Tokyo Medical Center, 2-5-1 Higashigaoka Meguro-ku, Tokyo, Japan. takaholy@aol.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural