Document Detail


Cardiac function and modulation of sarcomeric function by length.
MedLine Citation:
PMID:  18079105     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The Frank-Starling relationship provides beat-to-beat regulation of ventricular function by matching ventricular input and output. This review addresses the subcellular mechanisms by which the ventricle adjusts its output (i.e. stroke volume) by changes in end-diastolic volume. The subcellular processes are placed in the context of the four phases of the cardiac cycle with emphasis on the sarcomeric properties that mediate the number of force-generating cross-bridges recruited during pressure development. Additional mechanistic insight is provided regarding the factors that regulate myocyte loaded shortening speeds, which are paramount for dictating ejection volume. Emphasis is placed on the interplay between cross-bridge-induced cooperative activation of the thin filament and cooperative deactivation of the thin filament induced by muscle shortening. The balance of these two properties seems to determine systolic haemodynamics, and how this balance is modulated by sarcomere length, in part, underlies the Frank-Starling relationship.
Authors:
Laurin M Hanft; Fredrick S Korte; Kerry S McDonald
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review     Date:  2007-12-12
Journal Detail:
Title:  Cardiovascular research     Volume:  77     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2008 Mar 
Date Detail:
Created Date:  2008-02-25     Completed Date:  2008-08-29     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  627-36     Citation Subset:  IM    
Affiliation:
Department of Medical Pharmacology & Physiology, MA 415, Medical Sciences Building, School of Medicine, University of Missouri, Columbia, MO 65212, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Shape
Heart Failure / metabolism,  physiopathology
Humans
Microfilaments / metabolism
Models, Cardiovascular
Muscle Strength
Myocardial Contraction*
Myocardium / cytology,  metabolism*
Myocytes, Cardiac / metabolism
Myofibrils / metabolism
Sarcomeres / metabolism*
Stroke Volume
Ventricular Function, Left*
Ventricular Pressure
Grant Support
ID/Acronym/Agency:
AR 48523/AR/NIAMS NIH HHS; HL 057852/HL/NHLBI NIH HHS; HL 71550/HL/NHLBI NIH HHS

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


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