AJP - Heart Calcium Transients and Cell-Sarcomere
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 256: H1289-H1294, 1989;
0363-6135/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yasumura, Y.
Right arrow Articles by Suga, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yasumura, Y.
Right arrow Articles by Suga, H.

AJP - Heart and Circulatory Physiology, Vol 256, Issue 5 1289-H1294, Copyright © 1989 by American Physiological Society

ARTICLES

Minor preload dependence of O2 consumption of unloaded contraction in dog heart

Y. Yasumura, T. Nozawa, S. Futaki, N. Tanaka and H. Suga
Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.

We studied whether end-diastolic volume (EDV) would affect myocardial oxygen consumption (VO2) of mechanically unloaded contraction in the cross-circulated dog heart, as expected from the concept of the myocardial length-dependent activation. We made preloaded but maximally unloaded contractions from different EDVs by quickly releasing ventricular volume to eliminate systolic pressure development and hence to minimize the VO2 for mechanical load during the contraction. We then studied the relation between VO2 and EDV. The VO2 of the almost unloaded contraction from a relatively large EDV slightly exceeded the VO2 of the isovolumic contraction at V0, where V0 is the volume at which peak isovolumic pressure was zero. However, the excess VO2 could be ascribed to the residual systolic pressure-volume area (PVA) adversely produced from the large EDV, where PVA is a measure of the total mechanical energy generated during contraction. Therefore, we considered that VO2 was practically little dependent on EDV. We interpreted this finding as an indication that an increase, if any, in VO2 due to the length-dependent activation of the excitation-contraction coupling was practically negligible in the whole heart preparation.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
Y. Ohga, S. Sakata, C. Takenaka, T. Abe, T. Tsuji, S. Taniguchi, and M. Takaki
Cardiac dysfunction in terms of left ventricular mechanical work and energetics in hypothyroid rats
Am J Physiol Heart Circ Physiol, August 1, 2002; 283(2): H631 - H641.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
T. Abe, Y. Ohga, N. Tabayashi, S. Kobayashi, S. Sakata, H. Misawa, T. Tsuji, H. Kohzuki, H. Suga, S. Taniguchi, et al.
Left ventricular diastolic dysfunction in type 2 diabetes mellitus model rats
Am J Physiol Heart Circ Physiol, January 1, 2002; 282(1): H138 - H148.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online