Influence of Duraflo II heparin-treated extracorporeal circuits on the systemic inflammatory response in patients having coronary bypass.
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 after the leukocyte-endothelium interaction.
Department of Cardiothoracic Surgery, University Hospital Maastricht, The Netherlands.
P W
PW
Weerwind
J G
JG
Maessen
L J
LJ
van Tits
R K
RK
Stad
E J
EJ
Fransen
D S
DS
de Jong
O C
OC
Penn
D002315:Cardiopulmonary Bypass / Q000009:adverse effects / Q000295:instrumentation*; D001026:Coronary Artery Bypass; D019040:E-Selectin / Q000097:blood; D017558:Elective Surgical Procedures; D005260:Female; D006493:Heparin / Q000008:administration & dosage; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000517:prevention & control*; D018836:Inflammation Mediators / Q000097:blood*; D018799:Intercellular Adhesion Molecule-1 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D007962:Leukocytes / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D013499:Surface Properties
D019040:E-Selectin; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D018124:Receptors, Tumor Necrosis Factor; D018799:Intercellular Adhesion Molecule-1; D006493:Heparin