Document Detail

ET(A) receptor blockade improves post-ischaemic functional recovery in 'hibernating' rat myocardium.
MedLine Citation:
PMID:  12193089     Owner:  NLM     Status:  MEDLINE    
Endothelin-1 (ET-1) is a potent vasoconstrictor, and ET(A) receptors mainly mediate this effect. Elevated plasma levels of ET-1 are observed in patients with coronary heart disease. The release of this peptide from the damaged endothelium may play a role in the initiation and maintenance of myocardial ischaemia. This study examines the ET(A) receptor-mediated role of endogenous ET-1 in post-ischaemic myocardial function after prolonged hypoperfusion in normal non-failing hearts. In an isolated rat heart model for short-term myocardial hibernation, left ventricular functional recovery after 3 h of hypoperfusion (15% of pre-ischaemic flow) followed by 2 h of reperfusion was determined. Under steady-state conditions, coronary flow, left ventricular pressure (LVP) and dP/dt(max) were measured in the isovolumically beating heart. Additionally, the maximal inotropic response (LVP and dP/dt(max)) to calcium stimulation was determined. To study the role of ET(A) receptors under these pathophysiological conditions, one group was treated with the ET(A) antagonist BQ 610 (0.8 micromol/l) during hypoperfusion, and compared with a control group which received a saline infusion during hypoperfusion. Reperfusion for 2 h after 3 h of hypoperfusion resulted in partial functional recovery in both groups. Post-ischaemic recovery was significantly better in the hearts that were treated with the ET(A) antagonist BQ 610 during hypoperfusion (LVP, +19.5% compared with control; dP/dt(max), +13.7% compared with control). The inotropic response to calcium was nearly normalized after ET(A) blockade. Thus the normal non-failing myocardium profits from ET(A) receptor blockade during a prolonged period of hypoperfusion, resulting in significantly better post-ischaemic recovery of myocardial function.
Martin E Beyer; Marcus Fischer; Tobias Hövelborn; Hans Martin Hoffmeister
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  103 Suppl 48     ISSN:  0143-5221     ISO Abbreviation:  Clin. Sci.     Publication Date:  2002 Aug 
Date Detail:
Created Date:  2002-08-23     Completed Date:  2002-11-20     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  215S-218S     Citation Subset:  IM    
Medizinische Klinik, Abt. III, Eberhard-Karls-Universität, Otfried-Müller-Str. 10, 72076 Tübingen, Germany.
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MeSH Terms
Calcium / pharmacology
Endothelin-1 / metabolism*
Models, Animal
Myocardial Stunning / metabolism*
Myocardium / metabolism*
Oligopeptides / therapeutic use*
Rats, Wistar
Receptor, Endothelin A
Receptors, Endothelin / antagonists & inhibitors*
Sodium Chloride / pharmacology
Stimulation, Chemical
Time Factors
Reg. No./Substance:
0/Endothelin-1; 0/Oligopeptides; 0/Receptor, Endothelin A; 0/Receptors, Endothelin; 141595-53-1/BQ 610; 7440-70-2/Calcium; 7647-14-5/Sodium Chloride

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