The Thai Journal of Veterinary Medicine


Myocardial contractility is defined as the velocity of cycling of heavy meromyosin cross-bridges. Contractility may be defined also as the velocity of myocardial fiber shortening or change in ventricular dimension during contraction when the fiber shortens or the ventricle contracts against no load. In the clinic; however, myocardial contractility may be estimated by some parameters of systolic function adjusted for the degree of stretch on the fibers (the preload) just before contraction begins and the hindrance to ejection of blood (the afterload). Excitation-contraction coupling is a physicochemical process during which electrophysiological changes (initiated by depolarization of the cell) translate to mechanical changes (manifested as a combination of contraction and generation of tension). The result of this process is a combination of the ejection of blood out of the ventricle into and through the arterial tree and of the generation of pressure. Many indices have been used in both humans and experimental animals to assess cardiovascular function: (1) Vmax (the maximal velocity of fiber shortening estimated from the imaginary conditions of the fiber shortening against no load), (2) parameters (ESPVR, PRSW, Ees) obtained from the left ventricular pressure-volume relationship, (3) dLVP/dtmax (maximal rate of rise of left ventricular pressure), (4) QA interval (time between onset of electrical activity in the ventricle to initial elevation of arterial pressure), (5) ejection fraction (ratio of stroke volume to preload). However, some (3, 4 and 5) of these indices must be used with caution for estimating contractility since they are also influenced by other factors (e.g. preload, afterload, stiffness of the arterial tree). Parameters of the pressure-volume loop are considered the gold standard for measuring contractility, lusitrope, myocardial energetics and ventricular-vascular coupling.

First Page


Last Page