Document Detail


Morphine administration at reperfusion fails to improve postischaemic cardiac function but limits myocardial injury probably via heat-shock protein 27 phosphorylation.
MedLine Citation:
PMID:  19359990     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND OBJECTIVES: We explored the effects of morphine administration during reperfusion period after an index ischaemia as well as potential molecular mechanisms underlying this response. This is of important clinical value, as morphine is used routinely in cardiovascular anaesthesia and in the emergency management of cardiac infarction. METHODS: Male Wistar rat hearts, mounted on constant flow isolated Langendorff preparation, were subjected to stabilization, 30 min of zero-flow global ischaemia and 45 min of reperfusion (CONT; n = 10). Morphine (10(-6) mol l(-1)) was administered only at reperfusion (MORPH; n = 10). Postischaemic recoveries of left ventricular developed pressure were expressed as percentage of the initial value. At the end of the experimental protocol, lactate dehydrogenase release in the perfusate was measured and the left ventricle was isolated and used for determination of oxidized actin, mitogen-activated protein kinase activation and heat-shock protein 27 phosphorylation. RESULTS: Left ventricular developed pressure percentage did not differ between groups, whereas lactate dehydrogenase release was significantly reduced in MORPH compared with CONT hearts. Left ventricular developed pressure percentage was negatively correlated with lactate dehydrogenase release in CONT hearts (r = -0.8, P = 0.006), whereas in MORPH hearts no correlation was found (r = -0.2, P = 0.57). Phosphorylated p38 mitogen-activated protein kinase, c-jun N-terminal protein kinases, extracellular signal-regulated kinases and Akt at 45 min of reperfusion were similar between groups. However, a 1.5-fold increase in phospho-heat-shock protein 27 was found in MORPH hearts compared with CONT hearts (P < 0.05). Additionally, the ratio of oxidized actin to total actin was found to be 1.9-fold more in MORPH compared with CONT hearts (P < 0.05). CONCLUSION: Morphine administration at reperfusion does not affect cardiac function but limits the extent of myocardial injury, possibly through increased heat-shock protein 27 phosphorylation.
Authors:
Iordanis Mourouzis; Theodosios Saranteas; Philippos Perimenis; Christina Tesseromatis; Georgia Kostopanagiotou; Constantinos Pantos; Dennis V Cokkinos
Publication Detail:
Type:  In Vitro; Journal Article    
Journal Detail:
Title:  European journal of anaesthesiology     Volume:  26     ISSN:  1365-2346     ISO Abbreviation:  Eur J Anaesthesiol     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-10     Completed Date:  2009-08-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8411711     Medline TA:  Eur J Anaesthesiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  572-81     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, Attikon Hospital, University of Athens School of Medicine, Athens, Greece.
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MeSH Terms
Descriptor/Qualifier:
Actins / drug effects,  metabolism
Analgesics, Opioid / pharmacology*
Animals
Disease Models, Animal
HSP72 Heat-Shock Proteins / drug effects*,  metabolism
L-Lactate Dehydrogenase / metabolism
Male
Morphine / pharmacology*
Myocardial Reperfusion Injury / physiopathology*
Myocardium / pathology
Oxidation-Reduction
Phosphorylation / drug effects
Rats
Rats, Wistar
Chemical
Reg. No./Substance:
0/Actins; 0/Analgesics, Opioid; 0/HSP72 Heat-Shock Proteins; 57-27-2/Morphine; EC 1.1.1.27/L-Lactate Dehydrogenase

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