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


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
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):
Daniel R. Meldrum
Joseph C. Cleveland, Jr
Brian S. Cain
Alden H. Harken
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Meldrum, D. R.
Right arrow Articles by Harken, A. H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Meldrum, D. R.
Right arrow Articles by Harken, A. H.

Ann Thorac Surg 1998;65:439-443
© 1998 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Increased Myocardial Tumor Necrosis Factor-{alpha} in a Crystalloid-Perfused Model of Cardiac Ischemia-Reperfusion Injury

Daniel R. Meldrum, MD, Joseph C. Cleveland, Jr, , Brian S. Cain, MD, Xianzhong Meng, MD, PhD, Alden H. Harken, MD

Division of Cardiothoracic Surgery, Department of Surgery, University of Colorado Health Sciences Center, Denver, Colorado, USA

Accepted for publication August 8, 1997.

Dr Meldrum, Division of Cardiothoracic Surgery, University of Colorado Health Sciences Center, 4200 E Ninth Ave, Box C-306, Denver, CO 80262.

Background. The heart is a tumor necrosis factor-{alpha} (TNF-{alpha})–producing organ. Recent basic experimental and clinical evidence suggests that TNF-{alpha} is an important mediator of myocardial injury during acute myocardial infarction, chronic heart failure, cardiac allograft rejection, and cardiopulmonary bypass operations. Although it is known that the myocardium itself is capable of producing TNF-{alpha} in response to endotoxin, it is unknown whether there is an increase in myocardial tissue TNF-{alpha} levels after ischemia-reperfusion injury. We hypothesized that ischemia-reperfusion induces the production of TNF-{alpha} by the heart.

Methods. To avoid blood-borne TNF-{alpha} as a potentially confounding variable, we examined myocardial TNF-{alpha} production in a crystalloid-perfused model of cardiac ischemia-reperfusion injury. Isolated rat hearts were perfused with crystalloid solution and subjected to ischemia-reperfusion. Postischemic myocardial TNF-{alpha} was measured using an enzyme-linked immunosorbent assay and correlated with developed pressure, coronary flow, end-diastolic pressure, and creatine kinase loss (assay of activity in coronary effluent).

Results. Ischemia-reperfusion induced a marked increase in myocardial TNF-{alpha} that was associated with decreased myocardial contractility and coronary flow and with increased end-diastolic pressure and postischemic creatine kinase loss.

Conclusions. The heart produces TNF-{alpha} in response to ischemia-reperfusion. Ischemia-induced TNF-{alpha} production may contribute to postischemic myocardial stunning, necrosis, or both. Strategies designed to limit ischemia-induced myocardial TNF-{alpha} production may have therapeutic utility in the settings of planned myocardial ischemic events.






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 © 1998 by The Society of Thoracic Surgeons.