Force-frequency characteristics of the left ventricle in the conscious dog.
- 1 January 1978
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 42 (1) , 64-71
- https://doi.org/10.1161/01.res.42.1.64
Abstract
The early and late alterations in left ventricular function which follow a change in contraction frequency were assessed in 10 conscious dogs. Chronically implanted pulse-transit ultrasonic dimension transducers were used to measure the dynamic geometry of the left ventricle, and a high-fidelity micromanometer was employed to measure left ventricular pressure. The heart was paced from the atrium and, after every 20th regular beat, an extrasystole and a postextrasystole were introduced into the basic pacing rhythm. The ratio of the maximum derivative of left ventricular pressure (.ovrhdot.Pmax) of the postextrasystolic beat to the .ovrhdot.Pmax of the control beat was used as a measure of the degree of postextrasystolic potentiation of ventricular function. This postextrasystolic ratio was significantly influenced by the interval preceding the postextrasystolic beat; as this interval was increased, the end-diastolic volume and the .ovrhdot.Pmax of the postextrasystole also increased. When the end-diastolic geometry of the control and postextrasystolic beats were made identical, the postextrasystolic ratio reflected postextrasystolic potentiation of the inotropic state. The degree of postextrasystolic inotropic potentiation was a direct linear function of the change in contraction frequency induced by the extrasystole (r .gtoreq. 0.97). End-diastolic geometry and the magnitude of the frequency perturbation must be carefully controlled when postextrasystolic potentiation is used to evaluate left ventricular function. In contrast to postextrasystolic potentiation, steady state changes in contraction frequency did not significantly alter .ovrhdot.Pmax (P > 0.20). Significant decreases in end-diastolic volume were observed with increasing steady state heart rates (P < 0.05). This decrease in end-diastolic volume may be partially responsible for the lack of potentiation of steady state .ovrhdot.Pmax after a sustained increase in contraction frequency.This publication has 21 references indexed in Scilit:
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