Document Detail

Xenon induces late cardiac preconditioning in vivo: a role for cyclooxygenase 2?
MedLine Citation:
PMID:  19020121     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Xenon induces early myocardial preconditioning of the rat heart in vivo, but whether xenon induces late cardioprotection is not known. Cyclooxygenase-2 (COX-2) has been shown to be an important mediator in the signal transduction of myocardial ischemic late preconditioning (i-LPC). We investigated whether xenon induces late preconditioning (Xe-LPC) and whether COX-2 activity and/or expression are involved in mediating this effect. METHODS: Anesthetized male Wistar rats were instrumented with a coronary artery occluder. After 7 d of recovery, animals were randomized to 1 of 5 groups each containing 8 animals. The i-LPC group underwent 5 min of coronary occlusion to induce i-LPC. Xe-LPC was achieved by administration of xenon (70 volume%) for 15 min. Additional rats were pretreated with the COX-2 inhibitor NS-398 (5 mg kg(-1) body weight i.p.) with and without Xe-LPC. A group of sham operated animals not undergoing i-LPC or Xe-LPC served as controls (Con). After 24 h, all animals were anesthetized and underwent 25 min of myocardial ischemia induced by tightening of the coronary artery occluder followed by 2 h of reperfusion. Myocardial infarct size was assessed by triphenyltetrazolium chloride staining. In additional experiments, hearts were excised at different time points after preconditioning to investigate COX-2 mRNA and protein expression by polymerase chain reaction and infrared Western blot, respectively. RESULTS: Both i-LPC and Xe-LPC reduced myocardial infarct size (% of the area at risk) compared with Con (i-LPC: 29 +/- 7%; Xe-LPC 31 +/- 8%, both P < 0.05 vs Con 64 +/- 6%). NS-398 abolished the cardioprotective effect of Xe-LPC (61 +/- 6%, P < 0.05 vs Xe-LPC). COX-2 mRNA and protein expression was only increased in the i-LPC group, but not in the Xe-LPC group. CONCLUSION: Xenon induces late myocardial preconditioning that is abolished by functional blockade of COX-2 activity. In contrast to i-LPC, Xe-LPC did not lead to an increased expression of COX-2 mRNA and protein. These data suggest differences in COX-2 regulation in i-LPC and Xe-LPC.
Nina C Weber; Jan Frässdorf; Christoph Ratajczak; Yvonne Grueber; Wolfgang Schlack; Markus W Hollmann; Benedikt Preckel
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Anesthesia and analgesia     Volume:  107     ISSN:  1526-7598     ISO Abbreviation:  Anesth. Analg.     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-11-21     Completed Date:  2008-12-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  1310650     Medline TA:  Anesth Analg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1807-13     Citation Subset:  AIM; IM    
Laboratory of Experimental Intensive Care and Anesthesiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
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MeSH Terms
Cyclooxygenase 2 / analysis,  genetics,  physiology*
Heart Rate
Ischemic Preconditioning, Myocardial*
Myocardial Infarction / prevention & control
Nitrobenzenes / pharmacology
RNA, Messenger / analysis
Rats, Wistar
Sulfonamides / pharmacology
Xenon / pharmacology*
Reg. No./Substance:
0/Nitrobenzenes; 0/RNA, Messenger; 0/Sulfonamides; 123653-11-2/N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; 7440-63-3/Xenon; EC 2; EC protein, rat
Comment In:
Anesth Analg. 2008 Dec;107(6):1768-71   [PMID:  19020115 ]

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