Document Detail


Preconditioning with sevoflurane reduces changes in nicotinamide adenine dinucleotide during ischemia-reperfusion in isolated hearts: reversal by 5-hydroxydecanoic acid.
MedLine Citation:
PMID:  12552198     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Ischemia causes an imbalance in mitochondrial metabolism and accumulation of nicotinamide adenine dinucleotide (NADH). We showed that anesthetic preconditioning (APC), like ischemic preconditioning, improved mitochondrial NADH energy balance during ischemia and improved function and reduced infarct size on reperfusion. Opening adenosine triphosphate-sensitive potassium (K(atp)) channels may be involved in triggering APC. The authors tested if effects of APC on NADH concentrations before, during, and after ischemia are reversible by 5-hydroxydecanoate (5-HD), a putative mitochondrial K channel blocker. METHODS: Nicotinamide adenine dinucleotide fluorescence was measured in 60 guinea pig Langendorff-prepared hearts assigned into five groups: (1) no treatment before ischemia; (2) APC by exposure to 1.3 mm sevoflurane for 15 min; (3) 200 microm 5-HD from 5 min before to 15 min after sevoflurane exposure; (4) 35 min 5-HD alone; and (5) no treatment and no ischemia. Sevoflurane was washed out for 30 min, and 5-HD for 15 min, before 30-min ischemia and 120-min reperfusion. RESULTS: Nicotinamide adenine dinucleotide was reversibly increased during sevoflurane exposure before ischemia, and the increase and rate of decline in NADH during ischemia were reduced after APC. 5-HD abolished these changes in NADH. On reperfusion, function was improved and infarct size reduced after APC compared with other groups. CONCLUSION: Anesthetic preconditioning was evidenced by improved mitochondrial bioenergetics as assessed from NADH concentrations during ischemia and by attenuated reperfusion injury. Reversal of APC by bracketing sevoflurane exposure with 5-HD suggests that APC is triggered by mitochondrial K channel opening or, alternatively, by attenuated mitochondrial respiration without direct involvement of mitochondrial K channel opening.
Authors:
Matthias L Riess; Enis Novalija; Amadou K S Camara; Janis T Eells; Qun Chen; David F Stowe
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Anesthesiology     Volume:  98     ISSN:  0003-3022     ISO Abbreviation:  Anesthesiology     Publication Date:  2003 Feb 
Date Detail:
Created Date:  2003-01-28     Completed Date:  2003-02-25     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  1300217     Medline TA:  Anesthesiology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  387-95     Citation Subset:  AIM; IM    
Affiliation:
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226, USA.
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MeSH Terms
Descriptor/Qualifier:
ATP-Binding Cassette Transporters
Anesthetics, Inhalation / pharmacology*
Animals
Blood Pressure / drug effects
Coronary Circulation / drug effects
Decanoic Acids / pharmacology
Fluorescence
Guinea Pigs
Heart / drug effects
Hydroxy Acids / pharmacology
Ischemic Preconditioning, Myocardial*
Male
Methyl Ethers / pharmacology*
Mitochondria, Heart / drug effects
Myocardial Contraction / drug effects
Myocardial Infarction / pathology
Myocardial Ischemia / metabolism*
Myocardium / metabolism,  pathology
NAD / metabolism*
Potassium Channel Blockers / pharmacology
Potassium Channels / drug effects
Potassium Channels, Inwardly Rectifying
Ventricular Function, Left / drug effects
Grant Support
ID/Acronym/Agency:
ES06648/ES/NIEHS NIH HHS; HL58691/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/ATP-Binding Cassette Transporters; 0/Anesthetics, Inhalation; 0/Decanoic Acids; 0/Hydroxy Acids; 0/Methyl Ethers; 0/Potassium Channel Blockers; 0/Potassium Channels; 0/Potassium Channels, Inwardly Rectifying; 0/uK-ATP-1 potassium channel; 28523-86-6/sevoflurane; 53-84-9/NAD; 624-00-0/5-hydroxydecanoic acid

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


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