Faculty Collaboration Database

Preconditioning with sevoflurane reduces changes in nicotinamide adenine dinucleotide during ischemia-reperfusion in isolated hearts: reversal by 5-hydroxydecanoic acid. Anesthesiology 2003 Feb;98(2):387-95

Date

01/29/2003

Pubmed ID

12552198

DOI

10.1097/00000542-200302000-00019

Scopus ID

2-s2.0-0037318185 (requires institutional sign-in at Scopus site)   47 Citations

Abstract

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.

Author List

Riess ML, Novalija E, Camara AK, Eells JT, Chen Q, Stowe DF

Authors

Amadou K. Camara PhD Professor in the Anesthesiology department at Medical College of Wisconsin
Janis Eells PhD Professor in the Biomedical Sciences department at University of Wisconsin - Milwaukee
David F. Stowe MD, PhD Professor in the Anesthesiology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

ATP-Binding Cassette Transporters
Anesthetics, Inhalation
Animals
Blood Pressure
Coronary Circulation
Decanoic Acids
Fluorescence
Guinea Pigs
Heart
Hydroxy Acids
In Vitro Techniques
Ischemic Preconditioning, Myocardial
KATP Channels
Male
Methyl Ethers
Mitochondria, Heart
Myocardial Contraction
Myocardial Infarction
Myocardial Ischemia
Myocardium
NAD
Potassium Channel Blockers
Potassium Channels
Potassium Channels, Inwardly Rectifying
Ventricular Function, Left