Document Detail

Hyperoxia elicits myocardial protection through a nuclear factor kappaB-dependent mechanism in the rat heart.
MedLine Citation:
PMID:  12658209     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Hyperoxia has been previously shown to protect the heart from ischemia-reperfusion injury. In the present study we investigated whether the cardioprotective effects of hyperoxia were dependent on the redox-sensitive transcription factor nuclear factor kappaB. METHODS: Rats were kept in a hyperoxic (> or =95% O(2)) environment for 60 minutes. Their hearts were isolated immediately afterward, buffer perfused in a Langendorff apparatus, and subjected to 25 minutes of global ischemia and 60 minutes of reperfusion. Cardiac pressures and coronary flow were measured, and infarct size was determined by means of triphenyl tetrazolium chloride staining. Activation of nuclear factor kappaB was assessed by means of the electrophoretic mobility shift assay, whereas the inhibitor IkappaBalpha was evaluated by means of immunoblotting. Pharmacologic inhibition of nuclear factor kappaB was achieved with 2 different agents, SN50 and pyrrolidine dithiocarbamate. RESULTS: Preischemic exposure to hyperoxia improved postischemic recovery of myocardial contractile function and coronary flow and reduced infarct size. Hyperoxia activated pulmonary and myocardial nuclear factor kappaB. Pretreatment with SN50 (400 microg/kg administered intraperitoneally) or pyrrolidine dithiocarbamate (100 mg/kg administered intraperitoneally) before hyperoxia abolished the functional and infarct-limiting protection. Hyperoxia reduced nuclear factor kappaB activation in the heart during sustained ischemia and reperfusion and increased the cytoplasmatic inhibitory factor IkappaBalpha. Administration of pyrrolidine dithiocarbamate or SN50 during ischemia and reperfusion to isolated hearts from normoxic control animals improved postischemic contractile function and coronary flow and reduced infarct size. CONCLUSIONS: Hyperoxia protects the rat heart against ischemia-reperfusion injury. The cardioprotection depends on myocardial activation of the transcription factor nuclear factor kappaB. Our results support evidence for a dual role of nuclear factor kappaB in the heart.
Peeter Tähepõld; Jarle Vaage; Joel Starkopf; Guro Valen
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of thoracic and cardiovascular surgery     Volume:  125     ISSN:  0022-5223     ISO Abbreviation:  J. Thorac. Cardiovasc. Surg.     Publication Date:  2003 Mar 
Date Detail:
Created Date:  2003-03-26     Completed Date:  2003-04-25     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0376343     Medline TA:  J Thorac Cardiovasc Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  650-60     Citation Subset:  AIM; IM    
Crafoord Laboratory of Experimental Surgery, Karolinska Hospital, Stockholm, Sweden.
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MeSH Terms
Analysis of Variance
Antioxidants / pharmacology
Coronary Circulation
Disease Models, Animal*
Electrophoretic Mobility Shift Assay
Hyperoxia / metabolism*
I-kappa B Proteins / analysis
Ischemic Preconditioning, Myocardial / methods*
Myocardial Contraction
Myocardial Reperfusion Injury / metabolism*,  prevention & control*
NF-kappa B / analysis,  antagonists & inhibitors,  physiology*
Oxygen Inhalation Therapy / methods*
Peptides / pharmacology
Pyrrolidines / pharmacology
Rats, Sprague-Dawley
Recovery of Function
Thiocarbamates / pharmacology
Time Factors
Transcriptional Activation
Ventricular Pressure
Reg. No./Substance:
0/Antioxidants; 0/I-kappa B Proteins; 0/NF-kappa B; 0/Peptides; 0/Pyrrolidines; 0/SN50 peptide; 0/Thiocarbamates; 139874-52-5/NF-kappaB inhibitor alpha; 25769-03-3/pyrrolidine dithiocarbamic acid

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

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