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Author Solaro, R. John.

Title Regulation of cardiac contractility / R. John Solaro
Published San Rafael, CA : Morgan & Claypool Life Sciences, [2011]
©2011
Online access available from:
Colloquium Digital Library of Life Sciences    View Resource Record  

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Description 1 online resource (1 PDF file (vii, 35 pages : illustrations))
Series Integrated systems physiology, 2154-5626 ; no. 18
Colloquium series on integrated systems physiology ; no. 18. 2154-5626
Contents Introduction: Contractility and the Integrative Biology of the Myocardium -- Control of Contractility Is at the Cellular Level of Organization -- Left Ventricular Diastolic and Systolic Pressure, Ejection, and Relaxation Reflect Sarcomeric Mechanical Properties -- Integration of Sarcomere Mechanics with Cardiac Function Clarifies the Meaning of Preload, Afterload, and Contractility -- Pressure Volume Loops Provide a Quantification of Contractility -- Phosphorylations of Regulatory Proteins in Excitation Contraction Coupling Modify Contractility by Controlling Cellular Ca2+ Fluxes, the Response of the Myofilaments to Ca2+, and the Kinetics of the Cross-Bridge Cycle -- Contractility May Be Altered by a Variety of Mechanisms Not Involving a Prominent Role for the Autonomic Nervous System -- Cardiac Function Curves Provide a Compact Graphical Representation of Regulation of CO and SV -- Heart Failure as a Failure of Contractility
Summary Contractility describes the relative ability of the heart to eject a stroke volume (SV) at a given prevailing afterload (arterial pressure) and preload (end-diastolic volume; EDV). Various measures of contractility are related to the fraction as the SV/EDV or the ejection fraction, and the dynamics of ejection as determined from maximum pressure rise in the ventricles or arteries or from aortic flow velocities determined by echocardiography. At the cellular level, the ultimate determinant of contractility is the relative tension generation and shortening capability of the molecular motors (myosin cross-bridges) of the sarcomeres as determined by the rates and extent of Ca activation, the turnover kinetics of the cross-bridges, and the relative Ca responsiveness of the sarcomeres. Engagement of the regulatory signaling cascades controlling contractility occurs with occupancy and signal transduction by receptors for neurohumors of the autonomic nervous system as well as growth and stress signaling pathways. Contractility is also determined by the prevailing conditions of pH, temperature, and redox state. Short-term control of contractility is fully expressed during exercise. In long-term responses to stresses on the heart, contractility is modified by cellular remodeling and altered signaling that may compensate for a time but which ultimately may fail, leading to disorders
Analysis Afterload
Ca regulation
Heart
Length-dependent activation
Preload
Protein phosphorylation
Sarcomere
Notes Title from PDF t.p
Bibliography Includes bibliographical references
Notes Issued also in print
Mode of access: Internet
Subject Heart -- Contraction -- Regulation.
Myocardial Contraction -- physiology.
Calcium Signaling -- physiology.
Calcium -- metabolism.
Hemodynamics -- physiology.
Myocardium -- cytology.
Myocardium -- metabolism.
Form Electronic book
ISBN 1615041745 (paperback)
1615041753 (ebook)
9781615041749 (paperback)
9781615041756 (ebook)