Mechanoenergetics of negative inotropism of ventricular wall vibration in dog heart. Nishioka, Takehiko, Yoichi Goto, Katsuya Hata, Toshiyuki Takasago, Akio Saeki, Tad W. Taylor, and Hiroyuki Suga. Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, 5 Fujishirodai, Suita, Osaka, 565, and Department of Physiology II, Okayama University Medical School, Shikatacho, Okayama, 700 Japan
APStracts 2:0320H, 1995.
Mechanical vibration depresses cardiac contractility. We studied the mechanoenergetic effects of this negative inotropism in the left ventricle (LV) of the isolated cross-circulated dog heart preparation. We took full advantage of the mechanoenergetic relationship among the LV end-systolic elastance (Emax, contractility index), systolic pressure-volume area (PVA) and myocardial oxygen (O2) consumption (Vo2). PVA is a measure of the total mechanical energy that cardiac contraction generates. PVA correlates closely with Vo2. The Vo2 intercept of the Vo2-PVA relation reflects the Vo2 component for the excitation-contraction (E-C) coupling plus basal metabolism (PVA-independent Vo2). Vo2 above the PVA-independent Vo2 reflects the Vo2 component for mechanical contraction (PVA-dependent Vo2). When we applied 70 Hz vibration of 2 mm in amplitude to a LV wall region, it instantly decreased Emax and PVA by 20%, followed by a 10% decrease in Vo2 at a fixed volume. However, the vibration neither lowered the Vo2-PVA relation obtained at different LV volumes unlike the ordinary negative inotropism nor changed its slope [(1.88 0.23) vs. (1.86 0.23) x 10-5 ml O2[beta] mmHg-1.ml-1]. The virtually zero D(PVA-independent Vo2)/DEmax with the vibration indicates a much smaller O2 cost of Emax than calcium and propranolol. These mechanoenergetics support the hypothesis that mechanical vibration primarily suppresses cardiac contractility without suppressing the E -C coupling. 

Received 19 December 1994; accepted in final form 21 July 1995.
APS Manuscript Number H1107-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 August 1995.