Document Detail

Effects of sustained length-dependent activation on in situ cross-bridge dynamics in rat hearts.
MedLine Citation:
PMID:  17766361     Owner:  NLM     Status:  MEDLINE    
The cellular basis of the length-dependent increases in contractile force in the beating heart has remained unclear. Our aim was to investigate whether length-dependent mediated increases in contractile force are correlated with myosin head proximity to actin filaments, and presumably the number of cross-bridges activated during a contraction. We therefore employed x-ray diffraction analyses of beat-to-beat contractions in spontaneously beating rat hearts under open-chest conditions simultaneous with recordings of left ventricle (LV) pressure-volume. Regional x-ray diffraction patterns were recorded from the anterior LV free wall under steady-state contractions and during acute volume loading (intravenous lactate Ringers infusion at 60 ml/h, <5 min duration) to determine the change in intensity ratio (I(1,0)/I(1,1)) and myosin interfilament spacing (d(1,0)). We found no significant change in end-diastolic (ED) intensity ratio, indicating that the proportion of myosin heads in proximity to actin was unchanged by fiber stretching. Intensity ratio decreased significantly more during the isovolumetric contraction phase during volume loading than under baseline contractions. A significant systolic increase in myosin head proximity to actin filaments correlated with the maximum rate of pressure increase. Hence, a reduction in interfilament spacing at end-diastole ( approximately 0.5 nm) during stretch increased the proportion of cross-bridges activated. Furthermore, our recordings suggest that d(1,0) expansion was inversely related to LV volume but was restricted during contraction and sarcomere shortening to values smaller than the maximum during isovolumetric relaxation. Since ventricular volume, and presumably sarcomere length, was found to be directly related to interfilament spacing, these findings support a role for interfilament spacing in modulating cross-bridge formation and force developed before shortening.
James T Pearson; Mikiyasu Shirai; Hirotsugu Tsuchimochi; Daryl O Schwenke; Takayuki Ishida; Kenji Kangawa; Hiroyuki Suga; Naoto Yagi
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2007-08-31
Journal Detail:
Title:  Biophysical journal     Volume:  93     ISSN:  1542-0086     ISO Abbreviation:  Biophys. J.     Publication Date:  2007 Dec 
Date Detail:
Created Date:  2007-11-29     Completed Date:  2008-01-16     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  0370626     Medline TA:  Biophys J     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4319-29     Citation Subset:  IM    
Department of Cardiac Physiology, National Cardiovascular Center Research Institute, Suita, Osaka 565-8565, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Blood Pressure / physiology*
Calcium / metabolism*
Computer Simulation
Heart Ventricles / anatomy & histology*
Myocardial Contraction / physiology*
Rats, Sprague-Dawley
Sarcomeres / physiology*,  ultrastructure*
Ventricular Function*
Reg. No./Substance:
Comment In:
Biophys J. 2007 Dec 15;93(12):4095-6   [PMID:  17766360 ]

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

Previous Document:  Dynamics of learning in cultured neuronal networks with antagonists of glutamate receptors.
Next Document:  Elasticity of short DNA molecules: theory and experiment for contour lengths of 0.6-7 microm.