Author:
Solaro, R. John.
Imprint:San Rafael, Calif. (1537 Fourth Street, San Rafael, CA 94901 USA) : Morgan & Claypool, c2011.
Description1 electronic text (vii, 35 p.) : ill., digital file.
Note:Part of: Colloquium digital library of life sciences.
Note:Series from website.
Note:Introduction: contractility and the integrative biology of the myocardium -- Contractility in the modern context -- Control of cardiac contractility is critical to the matching of cardiac output to venous return during exercise with little change in end diastolic volume and with tuning of the dynamics of contraction and relaxation to heart rate -- 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 -- References -- Author biography.
Bibliography Note:Includes bibliographical references (p. 33).
Note: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.
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