| Cardiac function and modulation of sarcomeric function by length. | |
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MedLine Citation:
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PMID: 18079105 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Laurin M Hanft; Fredrick S Korte; Kerry S McDonald |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2007-12-12 |
Journal Detail:
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Title: Cardiovascular research Volume: 77 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 2008 Mar |
Date Detail:
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Created Date: 2008-02-25 Completed Date: 2008-08-29 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: Netherlands |
Other Details:
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Languages: eng Pagination: 627-36 Citation Subset: IM |
Affiliation:
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Department of Medical Pharmacology & Physiology, MA 415, Medical Sciences Building, School of Medicine, University of Missouri, Columbia, MO 65212, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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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