Document Detail


Existence of the Frank-Starling mechanism in the failing human heart. Investigations on the organ, tissue, and sarcomere levels.
MedLine Citation:
PMID:  8772688     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: The Frank-Starling mechanism is one of the most important physiological principles for regulation of contractile performance. We therefore studied the question of whether this mechanism may be absent or attenuated in end-stage failing human left ventricular myocardium. METHODS AND RESULTS: Different methodological approaches were used to analyze the effects of this mechanism on the organ, tissue, and sarcomere levels: (1) In excised human whole left ventricles (2 donor hearts, 5 failing hearts), diastolic and systolic pressure-volume relationships were obtained. (2) In isolated muscle strip preparations from the left ventricular wall of donor hearts (n = 14) and failing hearts from patients with idiopathic dilated cardiomyopathy (n = 21) and ischemic cardiomyopathy (n = 11), peak developed force was measured at different muscle lengths of the preparation. (3) Skinned fiber preparations were obtained from failing right and left ventricles (n = 12). In all three studies, we clearly observed the existence of the Frank-Starling mechanism: (1) In isolated failing human left ventricles, peak developed isometric pressure is increased when the preload is elevated. (2) Peak developed tension is increased by approximately 50% to 70% (P < .01) in left ventricular preparations of failing and nonfailing ventricles when the muscles are stretched from 90% to 100% optimum length. (3) An increase in sarcomere length leads to a sensitization of contractile proteins of ventricular skinned fiber preparations from failing human hearts. At 1.9-microns sarcomere length, the EC50 value was 5.56 +/- 0.06, and at 2.3 microns it was 5.70 +/- 0.05 (P < .01; n = 7). CONCLUSIONS: The Frank-Starling mechanism is maintained in end-stage failing human hearts, whereas significant alterations of diastolic myocardial distensibility are evident in chronic heart failure.
Authors:
C Holubarsch; T Ruf; D J Goldstein; R C Ashton; W Nickl; B Pieske; K Pioch; J Lüdemann; S Wiesner; G Hasenfuss; H Posival; H Just; D Burkhoff
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Circulation     Volume:  94     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1996 Aug 
Date Detail:
Created Date:  1996-10-10     Completed Date:  1996-10-10     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  683-9     Citation Subset:  AIM; IM    
Affiliation:
University of Freiburg, Department of Cardiology and Angiology, Germany.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Cardiomyopathy, Dilated / physiopathology*,  surgery
Diastole
Heart / physiology,  physiopathology*
Heart Failure / physiopathology*
Heart Transplantation
Heart Ventricles
Humans
Models, Cardiovascular
Muscle Fibers, Skeletal / physiology
Myocardial Contraction*
Reference Values
Sarcomeres / physiology*
Stroke Volume
Systole

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


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