Document Detail


Thrombin inhibitor reduces myocardial infarction in apoE-/- x LDLR-/- mice.
MedLine Citation:
PMID:  15031124     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We have previously shown that atherosclerotic apolipoprotein E-deficient (apoE(-/-)) x LDL receptor-deficient (LDLR(-/-)) mice develop myocardial infarction when exposed to hypoxic stress. This study was performed to assess the role of thrombin and thrombosis in this process. ApoE(-/-) x LDLR(-/-) mice were fed a cholesterol-rich diet for 8 mo and were then subjected to hypoxic stress while receiving isoflurane anesthesia. One group received a bolus dose (5.6 micromol/kg) of the thrombin inhibitor melagatran, and control animals received PBS 10 min before the hypoxic stress. The mice were exposed to 10 min of hypoxia followed by normoxia. Ten minutes after the stress, Alzet pumps delivering melagatran (20 nmol x kg x (-1)min(-1)) or PBS were implanted, and the mice were allowed to recover for 48 h. The cardiac response was analyzed by histology, immunohistochemistry, and serum troponin T assay. All animals showed reversible ECG changes as a sign of ischemia during hypoxic stress, and 50% developed infarctions afterward as judged by troponin T levels. The group that received thrombin inhibitor had significantly lower troponin T and smaller myocardial infarctions than the PBS-treated group. These data show that thrombin generation is an important pathogenetic factor and suggest that coronary thrombosis is involved in myocardial infarction in atherosclerotic mice. Exposure of atherosclerotic mice to hypoxia leads to myocardial infarction through a two-phase pathway in which acute transient ischemia is followed by thrombin-dependent, irreversible, myocardial ischemia and myocardial cell death.
Authors:
Anne-Louise Hemdahl; Erling Falk; Peter Thorén; Göran K Hansson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-03-18
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  287     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2004 Aug 
Date Detail:
Created Date:  2004-07-27     Completed Date:  2004-09-03     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H872-7     Citation Subset:  IM    
Affiliation:
Department of Medicine, Karolinska Institute, SE-171 76, Stockholm, Sweden.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apolipoproteins E / deficiency*
Azetidines
Benzylamines
Biological Markers / analysis
Coronary Artery Disease / metabolism,  pathology
Coronary Thrombosis / metabolism,  pathology
Electrocardiography
Glycine / analogs & derivatives*,  pharmacology*
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Infarction / diagnosis,  metabolism,  pathology*
Myocardium / metabolism,  pathology
Receptors, LDL / deficiency*
Thrombin / antagonists & inhibitors*
Troponin T / metabolism
Chemical
Reg. No./Substance:
0/Apolipoproteins E; 0/Azetidines; 0/Benzylamines; 0/Biological Markers; 0/Receptors, LDL; 0/Troponin T; 159776-70-2/melagatran; 56-40-6/Glycine; EC 3.4.21.5/Thrombin

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


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