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J Thorac Cardiovasc Surg 1995;110:1633-1641
© 1995 Mosby, Inc.


CARDIOPULMONARY BYPASS,
MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

INFLUENCE OF DURAFLO II HEPARIN-TREATED EXTRACORPOREAL CIRCUITS ON THE SYSTEMIC INFLAMMATORY RESPONSE IN PATIENTS HAVING CORONARY BYPASS

P. W. Weerwind, BSc, EKPa, J. G. Maessen, MD, PhDb, L. J. H. van Tits, PhDc, R. K. Stad, PhDc, E. J. Fransen, MScb, D. S. de Jong, CCPa, O. C. K. M. Penn, MD, PhDb


Maastricht, The Netherlands

Received for publication Jan. 3, 1995. Accepted for publication April 12, 1995. Address for reprints: J. G.Maessen, MD, PhD, Department of Cardiothoracic Surgery, University Hospital Maastricht, P.O. Box 5800, 6202 AZ Maastricht, The Netherlands.

Abstract

Cardiopulmonary bypass generates a systemic inflammatory response, including the activation of leukocytes, contributing to postoperative morbidity. To evaluate whether the use of heparin-treated extracorporeal circuits could reduce the inflammatory reaction in patients undergoing cardiopulmonary bypass, we conducted a prospective clinical study on 14 patients having coronary artery bypass in whom perfusion was done randomly with either Duraflo II heparin-treated circuits or with nontreated circuits. In both groups systemic heparinization was performed before cardiopulmonary bypass. The use of heparin-treated circuits resulted in a reduction of systemic inflammatory activation during cardiopulmonary bypass. This was reflected by lower plasma levels of soluble tumor necrosis factor receptors (p <0.05) and of interleukin-6 and interleukin-8 (p <0.05), manifest after release of the aortic crossclamp. Furthermore, 6 and 12 hours after aortic crossclamp release significantly lower levels of the soluble E-selectin (p <0.05) were observed in the Duraflo II group. In patients in whom noncoated circuits were used, a significant decrease in circulating soluble intercellular adhesion molecule 1 (p <0.05) was found early during bypass. All these observations suggest that the use of a heparin-treated extracorporeal circuit reduces the systemic inflammatory activation and may alter the leukocyte-endothelium interaction. (J THORAC CARDIOVASC SURG 1995;110:1633-41)




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