Document Detail


N-acetylcysteine restores isoflurane-induced preconditioning against myocardial infarction during hyperglycemia.
MedLine Citation:
PMID:  12766647     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Hyperglycemia generates reactive oxygen species and prevents isoflurane-induced preconditioning. The authors tested the hypothesis that scavenging reactive oxygen species with N-acetylcysteine will restore protection against myocardial infarction produced by isoflurane in vivo. METHODS: Barbiturate-anesthetized dogs (n = 45) were instrumented for measurement of systemic hemodynamics. Myocardial infarct size and coronary collateral blood flow were measured with triphenyltetrazolium staining and radioactive microspheres, respectively. All dogs were subjected to a 60-min left anterior descending coronary artery occlusion followed by 3 h of reperfusion. Dogs were randomly assigned to receive an infusion of 0.9% saline or 15% dextrose in water to increase blood glucose concentrations to 600 mg/dl (hyperglycemia) in the absence or presence of isoflurane (1.0 minimum alveolar concentration) with or without pretreatment with N-acetylcysteine (150 mg/kg i.v.) in six experimental groups. Isoflurane was discontinued, and blood glucose concentrations were allowed to return to baseline values before left anterior descending coronary artery occlusion. RESULTS: Myocardial infarct size was 27 +/- 2% (n = 8) of the left ventricular area at risk in control experiments. Isoflurane significantly (P < 0.05) decreased infarct size (13 +/- 2%; n = 7). Hyperglycemia alone did not alter infarct size (29 +/- 3%; n = 7) but abolished the protective effect of isoflurane (25 +/- 2%; n = 8). N-Acetylcysteine alone did not affect infarct size (28 +/- 2%; n = 8) but restored isoflurane-induced cardioprotection during hyperglycemia (10 +/- 1%; n = 7). CONCLUSIONS: Acute hyperglycemia abolishes reductions in myocardial infarct size produced by isoflurane, but N-acetylcysteine restores these beneficial effects. The results suggest that excessive quantities of reactive oxygen species generated during hyperglycemia impair isoflurane-induced preconditioning in dogs.
Authors:
Franz Kehl; John G Krolikowski; Dorothee Weihrauch; Paul S Pagel; David C Warltier; Judy R Kersten
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Anesthesiology     Volume:  98     ISSN:  0003-3022     ISO Abbreviation:  Anesthesiology     Publication Date:  2003 Jun 
Date Detail:
Created Date:  2003-05-26     Completed Date:  2003-06-24     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  1300217     Medline TA:  Anesthesiology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1384-90     Citation Subset:  AIM; IM    
Affiliation:
Department of Anesthesiology, Medical College of Wisconsin and the Zablocki VA Medical Center, Milwaukee, Wisconsin 53226, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetylcysteine / pharmacology*
Anesthetics, Inhalation / pharmacology*
Animals
Collateral Circulation / drug effects
Coronary Circulation / drug effects
Dogs
Female
Free Radical Scavengers / pharmacology*
Hemodynamics / drug effects
Hyperglycemia / complications*
Ischemic Preconditioning, Myocardial*
Isoflurane / pharmacology*
Male
Myocardial Infarction / etiology,  pathology,  prevention & control*
Myocardium / pathology
Ventricular Function, Left / drug effects
Grant Support
ID/Acronym/Agency:
GM-08377/GM/NIGMS NIH HHS; HL-036900/HL/NHLBI NIH HHS; HL-54820/HL/NHLBI NIH HHS; HL-63705/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Anesthetics, Inhalation; 0/Free Radical Scavengers; 26675-46-7/Isoflurane; 616-91-1/Acetylcysteine

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


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