JTCS Tips for Better Browsing
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
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 Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Yaku, H.
Right arrow Articles by Suga, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yaku, H.
Right arrow Articles by Suga, H.

The Journal of Thoracic and Cardiovascular Surgery, Vol 103, 514-520, Copyright © 1992 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Ventricular fibrillation does not depress postfibrillatory contractility in blood-perfused dog hearts

H Yaku, Y Goto, S Futaki, Y Ohgoshi, O Kawaguchi and H Suga
Department of Cardiovascular Dynamics, National Cardiovascular Center Research Institute, Osaka, Japan.

We studied whether ventricular fibrillation depresses ventricular contractility in a blood-perfused heart. In 12 excised, cross- circulated dog hearts, we measured left ventricular pressure and myocardial oxygen consumption at a middle left ventricular volume as control and induced ventricular fibrillation electrically. Six hearts were subjected to 20 minutes of ventricular fibrillation (group A), and the other six hearts were subjected to 40 minutes of ventricular fibrillation (group B). Then we defibrillated the heart with direct current shock and measured left ventricular pressure, left ventricular volume, and myocardial oxygen consumption immediately, 10 minutes, 20 minutes, and 30 minutes after the defibrillation. Coronary perfusion pressure was maintained normal (around 100 mm Hg) by the arterial pressure of the support dog throughout each experiment. Ventricular contractility was quantified by the maximum value for the instantaneous pressure/volume ratio (Emax). Pooled data of both groups A and B showed that Emax immediately after defibrillation increased to 116% +/- 28% (p less than 0.05) of control level and Emax 10 minutes after defibrillation decreased to 84% +/- 17% (p less than 0.05) of control level. Then Emax recovered to the control level: 95% +/- 18% (p greater than 0.05) of control level at 20 minutes and 100% +/- 20% (p greater than 0.05) of control level at 30 minutes after defibrillation. Emax of group A was not different from that of group B at comparable measurement times after defibrillation. Changes in myocardial oxygen consumption per beat were in proportion to the changes in Emax. We conclude that ventricular fibrillation per se for 20 to 40 minutes does not depress postfibrillatory contractility when coronary blood perfusion is maintained normal in the dog left ventricle.


This article has been cited by other articles:


Home page
 J. Thorac. Cardiovasc. Surg.Home page
Y. Sawa, J. Schaper, M. Roth, K. Nagasawa, G. Ballagi, N. Bleese, and W. Schaper
Platelet-activating factor plays an important role in reperfusion injury in myocardiumEfficacy of platelet-activating factor receptor antagonist (CV-3988) as compared with leukocyte-depleted reperfusion
J. Thorac. Cardiovasc. Surg., November 1, 1994; 108(5): 953 - 959.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 1992 by The American Association for Thoracic Surgery.