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):
Harold L. Lazar
Yusheng Bao
Richard J. Shemin
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lazar, H. L.
Right arrow Articles by Shemin, R. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lazar, H. L.
Right arrow Articles by Shemin, R. J.

Ann Thorac Surg 1998;65:973-977
© 1998 The Society of Thoracic Surgeons

Soluble Complement Receptor Type I Limits Damage During Revascularization of Ischemic Myocardium

Harold L. Lazar, MDa, Takafumi Hamasaki, MDa, Yusheng Bao, MDb, Samuel Rivers, BSb, Sheilah A. Bernard, MDa, Richard J. Shemin, MDa

a Department of Cardiothoracic Surgery, Boston Medical Center, Boston, Massachusetts, USA
b Boston University School of Medicine, Boston, Massachusetts, USA

Accepted for publication October 13, 1997.

Address reprint requests to Dr Lazar, Department of Cardiothoracic Surgery, Boston Medical Center, 88 E Newton St, Suite B404, Boston, MA 02118

Background. This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium.

Methods. In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4 = normal to -1 = dyskinesia), and infarct size (area of necrosis versus area at risk).

Results. After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1% ± 0.09% versus 7.8% ± 0.04%, respectively; p < 0.002), less myocardial acidosis (-0.41 ± 0.03 versus -0.72 ± 0.03, respectively; p < 0.0001), higher wall motion scores (3.1 ± 0.09 versus 1.67 ± 0.16, respectively; p < 0.0001), and smaller infarct size (24.6% ± 2.0% versus 41% ± 1.3%, respectively; p < 0.0001).

Conclusions. Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium.






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.