ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Author home page(s):
Fred A. Crawford, Jr
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 Cox, M. H.
Right arrow Articles by Spinale, F. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cox, M. H.
Right arrow Articles by Spinale, F. G.

Ann Thorac Surg 1997;63:981-987
© 1997 The Society of Thoracic Surgeons

Original Article: Cardiovascular

Protective Effects of Adenosine on Myocyte Contractility During Cardioplegic Arrest

Monty H. Cox, BS, Seung-Jun O, MD, Latha Hebbar, MD, Rupak Mukherjee, PhD, Fred A. Crawford, Jr, MD, Francis G. Spinale, MD, PhD

Division of Cardiothoracic Surgery and Department of Anesthesiology, Medical University of South Carolina, Charleston, South Carolina

Accepted for publication October 19, 1996.

Background. Adenosine delivery to the left ventricular myocardium has been demonstrated to provide protective effects in the setting of ischemia and reperfusion. However, whether adenosine has direct protective effects on isolated myocytes in the setting of cardioplegic arrest was unclear.

Methods. Isolated porcine left ventricular myocytes were assigned to one of the following treatment groups: (1) cardioplegia: 24 mEq/L K+, 4°C for 2 hours followed by rewarming (cell media, 37°C; n = 29); (2) cardioplegia augmented with adenosine (1 to 200 µmol/L) followed by rewarming (n = 98); and (3) normothermic control (cell media, 37°C, 2 hours; n = 175). Myocyte contractility was measured by computer-aided videomicroscopy.

Results. Cardioplegic arrest and rewarming reduced myocyte shortening velocity compared with normothermic control (25.3 ± 2.5 µm/s versus 50.9 ± 1.4 µm/s, p < 0.05). Adenosine-augmented cardioplegic arrest improved myocyte contractility with rewarming in a concentration-dependent fashion. For example, cardioplegia augmented with 10 µmol/L adenosine improved myocyte shortening velocity by 33% (33.6 ± 3.0 µm/s versus 25.3 ± 2.5 µm/s, p < 0.05), whereas 200 µmol/L adenosine improved shortening velocity by 97% (49.9 ± 3.4 µm/s vs 25.3 ± 2.5 µm/s, p < 0.05) compared with conventional cardioplegia.

Conclusions. This study demonstrated concentration-dependent protective effects of adenosine-augmented cardioplegia on myocyte contractile function with subsequent reperfusion and rewarming. These results suggest that stimulation of putative myocyte adenosine receptors may provide enhanced protective effects on myocyte contractile processes during cardioplegic arrest.




This article has been cited by other articles:


Home page
 Ann. Thorac. Surg.Home page
F. G. Spinale
Cellular and molecular therapeutic targets for treatment of contractile dysfunction after cardioplegic arrest
Ann. Thorac. Surg., November 1, 1999; 68(5): 1934 - 1941.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
A. Jovanovic, J. R. Lopez, A. E. Alekseev, W. K. Shen, and A. Terzic
Adenosine Prevents K-Induced Ca2 Loading: Insight Into Cardioprotection During Cardioplegia
Ann. Thorac. Surg., February 1, 1998; 65(2): 586 - 586.
[Abstract] [Full Text] [PDF]


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 © 1997 by The Society of Thoracic Surgeons.