Action potential control of cardiac contractility.
The transient and/or sustained trans-sarcolemmal voltage induced zero to peak tension changes in cardiac contractility at any given level of diastolic dimensions and associated physical-chemical conditions establish the action potential as the predominant controller of cardiac contractility. Demonstration that the inotropic increases in peak tension effects of extra cellular [Ca++] occur and are determined by the duration and degree of positivity of the plateau phase of the action potential document the predominant role of this phase of the action potential relative to control of cardiac contractility. The large increases in peak tension induced by prolongation of the plateau phase of the action potential by interpolated stimuli (i.e., extrasystolic potentiation) and the immediate maximal peak tension following sustained contracture induced by sarcolemmal depolarization highlight this fact. The demonstration that this prolonged action potential induced maximal tension capability (peak inotropic state) of ventricular fibers can be achieved within a single cycle suggests an analogous technic would provide objective noninvasive measurements of the cardiac reserve of humans in health and disease. A potentially valuable measurement, the temporal resolution requirements of which, although beyond the scope of current three-dimensional imaging systems, is achievable with current state of the art technology. The unique experimental and clinical diagnostic value of such a system for noninvasive analogous measurements in humans with congenital and acquired cardiac abnormalities is as yet, however, not widely recognized. Hence, objective confirmation of the unique potential value of such a system awaits development of the required high fidelity [X,Y,Z (1 mm3 voxel) spatial and (10 ms)] temporal resolution capability system.
Wood
E H
EH
Department of Physiology and Biophysics, Mayo Graduate School of Medicine, Rochester, MN 55905, USA. wood.earl@mayo.edu
D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000266:history / Q000378:metabolism; D004558:Electric Stimulation; D004594:Electrophysiology / Q000266:history*; D049673:History, 20th Century; D006801:Humans; D066298:In Vitro Techniques; D009200:Myocardial Contraction / Q000502:physiology*; D010100:Oxygen / Q000266:history / Q000378:metabolism; D010477:Perfusion / Q000266:history / Q000295:instrumentation; D014481:United States
D010100:Oxygen; D002118:Calcium