Document Detail


Activation of adenosine-monophosphate-activated protein kinase abolishes desflurane-induced preconditioning against myocardial infarction in vivo.
MedLine Citation:
PMID:  20456976     Owner:  NLM     Status:  In-Data-Review    
Abstract/OtherAbstract:
OBJECTIVES: Myocardial ischemia is accompanied by a rapid activation of adenosine-monophosphate-activated protein kinase (AMPK). However, it is unclear whether this represents a potentially beneficial or detrimental event in the course of ischemic injury. The role of AMPK activation in the cardioprotective setting of desflurane-induced preconditioning has not been investigated to date. Hence, the current study was undertaken to address the role of AMPK activation during desflurane-induced preconditioning in vivo.
DESIGN: A prospective randomized vehicle-controlled study.
SETTING: A university research laboratory.
SUBJECTS: Male New Zealand white rabbits (n = 44).
INTERVENTIONS: The animals were subjected to a 30-minute coronary artery occlusion (CAO) followed by 3 hours of reperfusion. Desflurane (1.0 minimum alveolar concentration) was administered for 30 minutes and discontinued 30 minutes prior to CAO. Different groups of animals received the AMPK activator, 5-aminoimidazole-4-carboxamide-1-b-riboside (AICAR), alone or in combination with desflurane. Infarct size was determined gravimetrically; AMPK activity and myocardial glycogen content were measured using specific assays. Phosphorylation of the AMPK substrate, acetyl-CoA carboxylase, was assessed by immunoblotting. Data are mean ± standard error of the mean.
RESULTS: Desflurane significantly reduced the myocardial infarct size (36.7 ± 1.9%, p < 0.05) compared with the control group (61.6% ± 3.0%), concomitant with increased myocardial tissue levels of glycogen (2.09 ± 0.07 μg, p < 0.05). Activation of the AMPK by AICAR alone did not protect against ischemic injury (65% ± 3.3), but did abolish the cardioprotection elicited by desflurane (61.8% ± 4.2%) at the same time as increasing myocardial glycogen consumption (1.42 ± 0.15 μg/mL).
CONCLUSIONS: The results obtained show that the pharmacologic activation of AMPK abolishes cardioprotection elicited by desflurane.
Authors:
Christopher Lotz; Beate Fisslthaler; Andreas Redel; Thorsten M Smul; Jan Stumpner; Joanna Pociej; Norbert Roewer; Ingrid Fleming; Franz Kehl; Markus Lange
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Publication Detail:
Type:  Journal Article     Date:  2010-04-24
Journal Detail:
Title:  Journal of cardiothoracic and vascular anesthesia     Volume:  25     ISSN:  1532-8422     ISO Abbreviation:  J. Cardiothorac. Vasc. Anesth.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-01-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9110208     Medline TA:  J Cardiothorac Vasc Anesth     Country:  United States    
Other Details:
Languages:  eng     Pagination:  66-71     Citation Subset:  IM    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
Affiliation:
Department of Anesthesiology, Bayerische Julius-Maximilians-Universitaet, Würzburg, Germany.
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