Document Detail

Induction of heat-shock proteins enhances myocardial and endothelial functional recovery after prolonged cardioplegic arrest.
MedLine Citation:
PMID:  8279883     Owner:  NLM     Status:  MEDLINE    
The aim of this study was to investigate the role of heat-shock proteins after heat-shock stress on the post-ischemic recovery of cardiac mechanical and endothelial function following a prolonged cardiac arrest. Isolated working rat hearts were subjected to a cardioplegic arrest for 4 hours at 4 degrees C. Three groups (n = 8 in each) were studied: (1) control, (2) sham-treated, and (3) heat-shocked rats. Postischemic recovery of cardiac output and endothelial function (as percent of preischemic control values) was 57.8% +/- 2.8% and 20.8% +/- 3.9% in group 1, 50.9% +/- 4.0% and 26.3% +/- 5.9% in group 2, and 74.0% +/- 2.4% and 51.2% +/- 8.0% in group 3, respectively. Both postischemic myocardial and endothelial function were improved by heat stress.
M Amrani; J Corbett; N J Allen; J O'Shea; S Y Boateng; A J May; M J Dunn; M H Yacoub
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  The Annals of thoracic surgery     Volume:  57     ISSN:  0003-4975     ISO Abbreviation:  Ann. Thorac. Surg.     Publication Date:  1994 Jan 
Date Detail:
Created Date:  1994-02-10     Completed Date:  1994-02-10     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  15030100R     Medline TA:  Ann Thorac Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  157-60     Citation Subset:  AIM; IM    
Cardiothoracic Surgery Department, National Heart and Lung Institute, London, England.
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MeSH Terms
Cardiac Output
Heart Arrest, Induced*
Heat Exhaustion / metabolism*
Heat-Shock Proteins / metabolism*
Nitric Oxide / metabolism
Reg. No./Substance:
0/Heat-Shock Proteins; 10102-43-9/Nitric Oxide

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