Document Detail


Ischemic preconditioning decreases the reperfusion-related formation of hydroxyl radicals in a rabbit model of regional myocardial ischemia and reperfusion: the role of K(ATP) channels.
MedLine Citation:
PMID:  16036354     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The objective of this study was to assess the effects of ischemic preconditioning (IP) on hydroxyl free radical production in an in vivo rabbit model of regional ischemia and reperfusion. Another goal was to determine whether K(ATP) channels are involved in these effects. The hearts of anesthetized and mechanically ventilated New Zealand White rabbits were exposed through a left thoracotomy. After i.v. salicylate (100 mg/kg) administration, all animals underwent a 30-min stabilization period followed by 40 min of regional ischemia and 2 h of reperfusion. In the IP group, IP was elicited by 5 min of ischemia followed by 10 min of reperfusion (prior to the 40-min ischemia period). Glibenclamide, a K(ATP) channel blocker, was administered prior to the preconditioning stimulus. Infarct size was measured by 2,3,5-triphenyl tetrazolium chloride (TTC) staining. We quantified the hydroxyl-mediated conversion of salicylate to its 2,3 and 2,5-dihydroxybenzoate derivatives during reperfusion by high performance liquid chromatography coupled with electro-chemical detection.IP was evidenced by reduced infarct size compared to control animals: 22% vs. 58%, respectively. Glibenclamide inhibited this cardioprotective effect and infarct size was 53%. IP limited the increase in 2,3 and 2,5-dihydroxybenzoic acid to 24.3 and 23.8% above baseline, respectively. Glibenclamide abrogated this effect and the increase in 2,3 and 2,5-dihydroxybenzoic acid was 94.3 and 85% above baseline levels, respectively, similar to the increase in the control group. We demonstrated that IP decreased the formation of hydroxyl radicals during reperfusion. The fact that glibenclamide inhibited this effect, indicates that K(ATP) channels play a key role in this cardioprotective effect of IP.
Authors:
Jacob Raphael; Benjamin Drenger; Julia Rivo; Edi Berenshtein; Mordechai Chevion; Yaacov Gozal
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Free radical research     Volume:  39     ISSN:  1071-5762     ISO Abbreviation:  Free Radic. Res.     Publication Date:  2005 Jul 
Date Detail:
Created Date:  2005-07-22     Completed Date:  2005-10-25     Revised Date:  2009-11-03    
Medline Journal Info:
Nlm Unique ID:  9423872     Medline TA:  Free Radic Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  747-54     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology and Critical Care Medicine, Hadassah-Hebrew University Medical Center, Jerusalem, Israel.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / metabolism
Animals
Chromatography, High Pressure Liquid
Free Radical Scavengers / pharmacology
Glyburide / pharmacology
Hydroxyl Radical / metabolism*
Ischemic Preconditioning, Myocardial*
Myocardial Infarction / blood,  metabolism*,  prevention & control*
Myocardium / metabolism
Potassium Channel Blockers / pharmacology
Potassium Channels / metabolism*
Rabbits
Chemical
Reg. No./Substance:
0/Free Radical Scavengers; 0/Potassium Channel Blockers; 0/Potassium Channels; 10238-21-8/Glyburide; 3352-57-6/Hydroxyl Radical; 56-65-5/Adenosine Triphosphate

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