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

Citation
Pw. Weerwind et al., INFLUENCE OF DURAFLO-II HEPARIN-TREATED EXTRACORPOREAL CIRCUITS ON THE SYSTEMIC INFLAMMATORY RESPONSE IN PATIENTS HAVING CORONARY-BYPASS, Journal of thoracic and cardiovascular surgery, 110(6), 1995, pp. 1633-1641
Citations number
52
Categorie Soggetti
Respiratory System","Cardiac & Cardiovascular System",Surgery
ISSN journal
00225223
Volume
110
Issue
6
Year of publication
1995
Pages
1633 - 1641
Database
ISI
SICI code
0022-5223(1995)110:6<1633:IODHEC>2.0.ZU;2-O
Abstract
Cardiopulmonary bypass generates a systemic inflammatory response, inc luding the activation of leukocytes, contributing to postoperative mor bidity, 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 r andomly with either Duraflo II heparin-treated circuits or with nontre ated circuits, In both groups systemic heparinization was performed be fore cardiopulmonary bypass, The use of heparin-treated circuits resul ted in a reduction of systemic inflammatory activation during cardiopu lmonary bypass, This was reflected by lower plasma levels of soluble t umor necrosis factor receptors (p < 0.05) and of interleukin-6 and int erleukin-8 (p < 0.05), manifest after release of the aortic crossclamp , Furthermore, 6 and 12 hours after aortic crossclamp release signific antly lower levels of the soluble E-selectin (p < 0.05) were observed in the Duraflo II group, In patients in whom noncoated circuits were u sed, a significant decrease in circulating soluble intercellular adhes ion molecule 1 (p < 0.05) was found early during bypass. All these obs ervations suggest that the use of a heparin-treated extracorporeal cir cuit reduces the systemic inflammatory activation and may alter the le ukocyte-endothelium interaction.