Document Detail


Myocardial microvascular permeability, interstitial oedema, and compromised cardiac function.
MedLine Citation:
PMID:  20472566     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The heart, perhaps more than any other organ, is exquisitely sensitive to increases in microvascular permeability and the accumulation of myocardial interstitial oedema fluid. Whereas some organs can cope with profound increases in the interstitial fluid volume or oedema formation without a compromise in function, heart function is significantly compromised with only a few percent increase in the interstitial fluid volume. This would be of little consequence if myocardial oedema were an uncommon pathology. On the contrary, myocardial oedema forms in response to many disease states as well as clinical interventions such as cardiopulmonary bypass and cardioplegic arrest common to many cardiothoracic surgical procedures. The heart's inability to function effectively in the presence of myocardial oedema is further confounded by the perplexing fact that the resolution of myocardial oedema does not restore normal cardiac function. We will attempt to provide some insight as to how microvascular permeability and myocardial oedema formation compromise cardiac function and discuss the acute changes that might take place in the myocardium to perpetuate compromised cardiac function following oedema resolution. We will also discuss compensatory changes in the interstitial matrix of the heart in response to chronic myocardial oedema and the role they play to optimize myocardial function during chronic oedemagenic disease.
Authors:
Ranjeet M Dongaonkar; Randolph H Stewart; Hans J Geissler; Glen A Laine
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2010-05-13
Journal Detail:
Title:  Cardiovascular research     Volume:  87     ISSN:  1755-3245     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2010 Jul 
Date Detail:
Created Date:  2010-07-02     Completed Date:  2010-10-12     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  331-9     Citation Subset:  IM    
Affiliation:
Michael E. DeBakey Institute, Texas A&M University, College Station, TX 77843-4466, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Body Fluids / metabolism*
Capillary Permeability*
Coronary Vessels / metabolism*,  physiopathology
Diagnostic Imaging / methods
Edema, Cardiac / diagnosis,  metabolism*,  physiopathology
Hemodynamics
Humans
Microvessels / metabolism*,  physiopathology
Models, Cardiovascular
Myocardial Contraction
Myocardium / metabolism*
Predictive Value of Tests
Signal Transduction
Ventricular Function*
Grant Support
ID/Acronym/Agency:
R01 HL092916/HL/NHLBI NIH HHS
Comments/Corrections

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