Document Detail


Tissue factor and thrombin mediate myocardial ischemia-reperfusion injury.
MedLine Citation:
PMID:  12607707     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Reperfusion of the ischemic heart is necessary to prevent irreversible injury of the myocardium, which leads to permanent organ dysfunction. However, reperfusion in itself leads to myocardial ischemia/reperfusion (I/R) injury, which is characterized by an acute inflammatory response mediated by activated inflammatory cells, chemokines, cytokines, and adhesion molecules. The molecular mechanisms of myocardial I/R injury are not completely known. Tissue factor (TF) and thrombin, two potent procoagulant and proinflammatory mediators, are recognized to play significant roles in myocardial I/R injury. To investigate the role of TF and thrombin in myocardial I/R injury, we used rabbit and murine in situ coronary artery ligation models. Increased TF mRNA, antigen, and activity were found in ischemic cardiomyocytes. Administration of an inhibitory antirabbit TF monoclonal antibody before or during the onset of ischemia resulted in a significant reduction in infarct size. Functional inhibition of thrombin with hirudin also reduced the infarct size. However, defibrinogenating rabbits with ancrod had no effect on infarct size, suggesting a requirement of thrombin generation but not fibrin deposition in myocardial I/R injury.
Authors:
Albert J Chong; Timothy H Pohlman; Craig R Hampton; Akira Shimamoto; Nigel Mackman; Edward D Verrier
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  The Annals of thoracic surgery     Volume:  75     ISSN:  0003-4975     ISO Abbreviation:  Ann. Thorac. Surg.     Publication Date:  2003 Feb 
Date Detail:
Created Date:  2003-02-27     Completed Date:  2003-03-17     Revised Date:  2005-11-16    
Medline Journal Info:
Nlm Unique ID:  15030100R     Medline TA:  Ann Thorac Surg     Country:  United States    
Other Details:
Languages:  eng     Pagination:  S649-55     Citation Subset:  AIM; IM    
Affiliation:
Division of Cardiothoracic Surgery, The University of Washington, Seattle, Washington 98104, USA.
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MeSH Terms
Descriptor/Qualifier:
Ancrod / pharmacology
Animals
Antibodies, Monoclonal / pharmacology
Disease Models, Animal
Fibrinolytic Agents / pharmacology
Hirudins / pharmacology
Mice
Mice, Knockout
Myocardial Reperfusion Injury / pathology,  physiopathology*
Myocardium / ultrastructure
RNA, Messenger / analysis
Rabbits
Receptor, PAR-1
Receptors, Thrombin / physiology
Thrombin / physiology*
Thromboplastin / physiology*
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Fibrinolytic Agents; 0/Hirudins; 0/RNA, Messenger; 0/Receptor, PAR-1; 0/Receptors, Thrombin; 9035-58-9/Thromboplastin; EC 3.4.21.-/Ancrod; EC 3.4.21.5/Thrombin

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


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