HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): James K. Kirklin David C. McGiffin Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kirklin, J. K. Articles by McGiffin, D. C. Search for Related Content PubMed PubMed Citation Articles by Kirklin, J. K. Articles by McGiffin, D. C.

Ann Thorac Surg 1999;68:1978-1982
© 1999 The Society of Thoracic Surgeons

---

II. Surgical Myocardial Protection

Control of the inflammatory response in extended myocardial preservation of the donor heart

^a Division of Cardiothoracic Surgery, Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama, USA

Address reprint requests to Dr Kirklin, Department of Surgery, University of Alabama at Birmingham, 739 Zeigler Bldg, 703 So 19th St, Birmingham, AL 35294
e-mail: jkirklin{at}uab.edu

Presented at the International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, Sep 21–24, 1997.

Abstract

The damaging effects of inflammation after prolonged myocardial ischemia are typically manifest during the period of reperfusion. The imbalance between free radical generation and availability of natural free radical scavengers during postischemic reperfusion set the stage for free radical injury. Calcium overload may convert reversible ischemic damage to fatal myocyte contracture. Complement activation and neutrophil activation, adhesion, and diapedesis are central components of the damaging inflammatory response. Cytokines such as tumor necrosis factor and IL1 simulate IL8 synthesis which is also a potent chemoattractant for neutrophils. The endothelial contribution to ischemic-reperfusion injury results from an imbalance between the production of naturally occurring vasodilators, such as prostacycline and nitric oxide, and vasoconstrictor products, such as endothelin, thromboxane A2, and angiotensin 2. Knowledge of these basic mechanisms has stimulated the formulation of preservation solutions and strategies to ameliorate the inflammatory response during reperfusion.

This article has been cited by other articles:

				A. S. Wechsler and J. Y. Kresh Of Mice and Men (and Effects of Gene Silencing) Circulation, September 22, 2009; 120(12): 1027 - 1028. [Full Text] [PDF]

				T Kofidis, H Baraki, H Singh, H Kamiya, M Winterhalter, V Didilis, M Emmert, F Woitek, A Haverich, and U Klima The minimized extracorporeal circulation system causes less inflammation and organ damage Perfusion, May 1, 2008; 23(3): 147 - 151. [Abstract] [PDF]

				L. Dvorak, J. Pirk, S. Cerny, and J. Kovar The role of leukocyte depleting filters in heart transplantation: early outcomes in prospective, randomized clinical trial. Eur. J. Cardiothorac. Surg., October 1, 2006; 30(4): 621 - 627. [Abstract] [Full Text] [PDF]

				Y. Lamarche, J. Gagnon, O. Malo, G. Blaise, M. Carrier, and L. P. Perrault Ventilation prevents pulmonary endothelial dysfunction and improves oxygenation after cardiopulmonary bypass without aortic cross-clamping Eur. J. Cardiothorac. Surg., September 1, 2004; 26(3): 554 - 563. [Abstract] [Full Text] [PDF]

				G. Plenz, H. Eschert, M. Erren, T. Wichter, M. Bohm, M. Flesch, H. H. Scheld, and M. C. Deng The interleukin-6/interleukin-6-receptorsystem is activated in donor hearts J. Am. Coll. Cardiol., May 1, 2002; 39(9): 1508 - 1512. [Abstract] [Full Text] [PDF]

				S. C. Stoica, M. Goddard, and S. R. Large The endothelium in clinical cardiac transplantation Ann. Thorac. Surg., March 1, 2002; 73(3): 1002 - 1008. [Abstract] [Full Text] [PDF]