Document Detail


Increased formation of interstitial hydroxyl radical following myocardial ischemia: possible relationship to endogenous opioid peptides.
MedLine Citation:
PMID:  9754328     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The effects of myocardial ischemia and reperfusion on interstitial hydroxyl radical production, in the left ventricular myocardium of anesthetized cats, were investigated. Ringer's solution containing salicylic acid was perfused through an implanted microdialysis probe. Hydroxyl radical production was evaluated as the 2,3 and 2,5 dihydroxybenzoic acid (DHBA) concentrations in the microdialysates by an on-line high performance liquid chromatography system. Myocardial ischemia for 60 min, induced by ligation of the left anterior descending coronary artery, significantly increased both 2,3 and 2,5 DHBA levels when compared with the sham-operated cats. Naloxone (1 mg/kg, bolus, intravenous), an endogenous opioid peptide receptor antagonist, significantly suppressed the ischemia-induced production of hydroxyl radicals. Myocardial ischemia also induced cardiac arrhythmia. Naloxone reduced the severity of ischemia-induced arrhythmia, as observed by a significantly lower arrhythmia score (1.4 +/- 0.2 vs. 4.6 +/- 0.4 for control), and by diminished incidence of ventricular tachycardia (0/7 vs. 8/8 for control) and ventricular fibrillation (0/7 vs. 3/8 for control). Furthermore, perfusion of dynorphin (0.25 microgram, 2.5 micrograms and 25 micrograms), an endogenous opioid peptide receptor agonist, increased hydroxyl radical production. Our results suggest that, in anesthetized cats, myocardial ischemia can induce production of interstitial hydroxyl radical in left ventricular myocardium, and this production may involve the actions of released endogenous opioid peptides on their receptors.
Authors:
C S Yang; P J Tsai; W Y Chen; J S Kuo
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Redox report : communications in free radical research     Volume:  3     ISSN:  1351-0002     ISO Abbreviation:  Redox Rep.     Publication Date:    1997 Oct-Dec
Date Detail:
Created Date:  1998-10-23     Completed Date:  1998-10-23     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9511366     Medline TA:  Redox Rep     Country:  SCOTLAND    
Other Details:
Languages:  eng     Pagination:  295-301     Citation Subset:  IM    
Affiliation:
Department of Medical Research, Taichung Veterans General Hospital, Taiwan, R.O.C.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arrhythmias, Cardiac / etiology,  physiopathology,  prevention & control*
Cats
Gentisates*
Heart / drug effects
Hydroxybenzoic Acids / metabolism
Hydroxyl Radical / metabolism*
Male
Microdialysis
Myocardial Ischemia / complications,  metabolism*,  physiopathology
Myocardial Reperfusion*
Myocardium / metabolism*
Naloxone / pharmacology*
Reference Values
Tachycardia, Ventricular / etiology,  physiopathology,  prevention & control*
Chemical
Reg. No./Substance:
0/Gentisates; 0/Hydroxybenzoic Acids; 303-38-8/2-pyrocatechuic acid; 3352-57-6/Hydroxyl Radical; 465-65-6/Naloxone; 490-79-9/2,5-dihydroxybenzoic acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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