Document Detail


Postinfarction healing dynamics in the mechanically unloaded rat left ventricle.
MedLine Citation:
PMID:  21398590     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The healing process is a key determinant for postinfarction left ventricular (LV) remodeling and the development of heart failure, which could be influenced by mechanical (pressure and/or volume) load. So far, limited information exists regarding an indepth characterization of the postinfarct healing process in the mechanically unloaded state. In the present work, we performed isogenic Lewis-to-Lewis rat abdominal heterotopic heart transplantation, which is characterized by hemodynamic unloading in the left ventricle, and simultaneously ligated the left anterior descending coronary artery (T-infarct group). Pathological evolution was dynamically compared with that of in situ infarcted Lewis hearts (I-infarct group) on days 3, 7, 14, and 35. There was a remarkable myocardial salvage in the unloaded heart, as shown by the improvement in infarct size (T-infarct group: 25.47% ± 4.31% vs. I-infarct group: 38.46% ± 4.82%, P < 0.01) and the smaller fraction of fibrosis in infarct segments (T-infarct group: 42.12% ± 8.40% vs. I-infarct group: 75.65% ± 10.51%, P < 0.01). In addition, there was a progressive disorganization of the two-dimensional collagen fiber alignment as well as retarded collagen fiber maturation in the T-infarct group. We also observed enhanced angiogenesis, lymphangiogenesis, and inflammatory cell retention in the infarct region during mechanical unloading. Moreover, capillary density and collagen deposition were significantly increased in the noninfarcted area of the unloaded heart compared with the same region in the in situ infarcted heart. In conclusion, ischemic insult in the mechanically unloaded heart elicits an altered inflammatory and healing response, which is characterized by myocardial salvage, delayed resolution of inflammation, and disorganization of the collagen orientation in the infarcted region. These findings could provide novel insights into the contribution of hemodynamic load in the postinfarction healing process. Further studies are warranted to elucidate its potential mechanism.
Authors:
Xin Zhou; Ji-Li Yun; Zhi-Qi Han; Fei Gao; He Li; Tie-Min Jiang; Yu-Ming Li
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-03-11
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  300     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-05-02     Completed Date:  2011-07-07     Revised Date:  2013-06-30    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1863-74     Citation Subset:  IM    
Affiliation:
Institute of Cardiovascular Diseases and Division of Cardiology, Pingjin Hospital, Medical College of Chinese People's Armed Police Forces, Tianjin 300162, China. cardiolab@gmail.com
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MeSH Terms
Descriptor/Qualifier:
Animals
Collagen / metabolism
Coronary Vessels / physiopathology
Heart Transplantation
Hemodynamics / physiology*
Ligation
Male
Microcirculation / physiology
Models, Animal
Myocardial Infarction / metabolism,  physiopathology*
Rats
Rats, Inbred Lew
Stress, Mechanical*
Ventricular Remodeling / physiology*
Wound Healing / physiology*
Chemical
Reg. No./Substance:
9007-34-5/Collagen
Comments/Corrections

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


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