Document Detail


End-systolic pressure-volume relationship and intracellular control of contraction.
MedLine Citation:
PMID:  8769770     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The left ventricular (LV) pressure-volume relationship and the effect of ejection on pressure generation are predicted theoretically based on the intracellular control mechanisms. The control of contraction is described based on coupling calcium kinetics and cross-bridge cycling. The analysis of published skinned and intact cardiac muscle data suggests two feedback control loops: 1) a positive cooperative mechanism that determines the force-length relationship, the length dependence calcium sensitivity of the contractile filaments, and the related Frank Starling law; and 2) a negative mechanical feedback that determines the force-velocity relationship and the generated power. The interplay between these two feedback mechanisms explains the wide spectrum of phenomena associated with the end-systolic pressure-volume relationship (ESPVR); it provides an explanation for the "shortening deactivation" and for the recent observations of the positive effect of ejection on the ESPVR, i.e., the increase of the end-systolic pressure of the ejecting beat over the pressure of the isovolumic beat at the same end-systolic volume. Furthermore, the analysis suggests that the LV contractility depends on the balance between the two intracellular mechanisms and that the effect of loading conditions is determined through these intracellular mechanisms.
Authors:
A Landesberg
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of physiology     Volume:  270     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1996 Jan 
Date Detail:
Created Date:  1996-12-20     Completed Date:  1996-12-20     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H338-49     Citation Subset:  IM; S    
Affiliation:
Julius Silver Institute, Department of Biomedical Engineering, Technion-Israel Institute of Technology, Haifa, Israel.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure*
Humans
Intracellular Membranes / physiology*
Models, Cardiovascular*
Myocardial Contraction / physiology*
Stroke Volume*

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


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