Document Detail


Effects of propofol on ischemia-induced ventricular arrhythmias and mitochondrial ATP-sensitive potassium channels.
MedLine Citation:
PMID:  22983391     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
AIM: To investigate the potential of propofol in suppressing ventricular arrhythmias and to examine whether mitochondrial ATP-sensitive potassium channels are involved.
METHODS: Male Sprague-Dawley rats were pretreated with intravenous infusion of propofol (Prop), a selective mitochondrial KATP channel inhibitor 5-hydroxydecanoate (5-HD), propofol plus 5-HD (Prop+5-HD), a potent mitochondrial K(ATP) channel opener diazoxide (DZ) or NS, respectively. The dosage of each drug was 10 mg/kg. The animals then underwent a 30 min-ligation of the left anterior descending artery. The severity of arrhythmias, the incidence of ventricular fibrillation (VF), and the time of the first run of ventricular arrhythmias were documented using an arrhythmia scoring system. Mitochondrial membrane potential (ΔΨm) was measured in freshly isolated rat cardiomyocytes with a fluorescence microscope.
RESULTS: The arrhythmia scores in the Prop and DZ group were 2.6(0-5) and 2.4(0-5), respectively, which were significantly lower than that in the control group [4.9(2-8)]. VF was not observed in both Prop and DZ groups. The first run of ventricular arrhythmias was significantly postponed in the Prop group (10.5±2.2 vs 7.3±1.9 min). Bracketing of propofol with 5-HD eliminated the anti-arrhythmic effect of propofol. In isolated rat cardiomyocytes, propofol (50 μmol/L) significantly decreased ΔΨm, but when propofol was co-administered with 5-HD, the effect on ΔΨm was reversed.
CONCLUSION: Propofol preconditioning suppresses ischemia-induced ventricular arrhythmias in the rat heart, which are proposed to be caused by opening of mitochondrial K(ATP) channels.
Authors:
Qiang Liu; Jun-yan Yao; Cheng Qian; Rong Chen; Xiao-yu Li; Shao-wen Liu; Bao-gui Sun; Long-sheng Song; Jiang Hong
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2012-09-17
Journal Detail:
Title:  Acta pharmacologica Sinica     Volume:  33     ISSN:  1745-7254     ISO Abbreviation:  Acta Pharmacol. Sin.     Publication Date:  2012 Dec 
Date Detail:
Created Date:  2012-12-05     Completed Date:  2013-11-15     Revised Date:  2014-04-08    
Medline Journal Info:
Nlm Unique ID:  100956087     Medline TA:  Acta Pharmacol Sin     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1495-501     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cells, Cultured
Electrocardiography
Hemodynamics / drug effects
KATP Channels / antagonists & inhibitors,  metabolism*
Male
Membrane Potential, Mitochondrial / drug effects
Microscopy, Fluorescence
Mitochondria, Heart / drug effects*,  metabolism
Myocardial Ischemia / complications*,  drug therapy,  metabolism
Myocytes, Cardiac / drug effects,  metabolism
Propofol / administration & dosage,  pharmacology,  therapeutic use*
Rats
Rats, Sprague-Dawley
Ventricular Fibrillation / etiology,  metabolism,  prevention & control*
Chemical
Reg. No./Substance:
0/KATP Channels; YI7VU623SF/Propofol

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


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