Increasing ventricular tension development per unit of time leads to increased contractility (homeometric autoregulation), a phenomenon that is independent of changes in coronary flow.
Describes homeometric autoregulation, demonstrating that increased ventricular tension development leads to increased contractility independent of end-diastolic fiber length or coronary flow.
The effect of increasing the activity of the ventricle on its contractility was investigated. Several beats after the ventricle increases the amount of tension it develops per unit of time, it exhibits an increased contractility as shown by the increase in work and the more rapid development of pressure from a given end-diastolic pressure or fiber length. This has been termed homeometric autoregulation in contradistinction to the Frank-Starling or heterometric type of autoregulation. It was found that changes in coronary flow are not essential to the exhibition of this phenomenon. Possible mechanisms and the physiologic significance of the findings are discussed.
Sarnoff et al. (1960) studied this question. Increasing ventricular tension development was evaluated on Ventricular contractility (work and rate of pressure development). Increasing ventricular tension development per unit of time leads to increased contractility (homeometric autoregulation), a phenomenon that is independent of changes in coronary flow.