Duroflo II heparin bonding does not attenuate cytokine release or improve pulmonary function.
BACKGROUND
Comparison of the cytokine generation and leukocyte activation properties of Duroflo II heparin bonded bypass circuit (Baxter Healthcare Corp, Compton, UK) and the conventional cardiopulmonary bypass circuit. Attempt to correlate these to pulmonary dysfunction postoperatively.


METHODS
Forty patients undergoing elective, isolated coronary artery bypass grafting were randomly allocated to have either plain extracorporeal circuits (group C) or heparin bonded extracorporeal circuits (group H). Full systemic heparinization was used in all patients. The inflammatory response was assessed by measuring plasma levels of interleukin-6, interleukin-8, interleukin-10, and polymorphonuclear elastase. Gas exchange was assessed by measuring the PaO2/FIO2 ratio.


RESULTS
Significant impairment of oxygenation was seen in both groups with the lowest values at the end of the operation before a gradual return to normal during the next 6 hours. There were no differences between the groups in gas exchange or times to extubation. There were significant elevations in all the cytokines, with interleukin-6 levels peaking at 4 hours in group H and 24 hours in group C, before starting to return to normal at 48 hours. The patterns of interleukin-8 and interleukin-10 rise were identical in the two groups. Polymorphonuclear elastase reached a peak at the end of the operation in group H and remained elevated up to 24 hours, whereas levels continued to rise in group C up to 4 hours. There were no significant differences in levels between groups at any time. There were no differences between the groups in blood loss or blood product usage.


CONCLUSIONS
Cardiopulmonary bypass induces a systemic inflammatory response with release of cytokines and activation of leukocytes. This correlates with the severe deterioration in pulmonary gas exchange from preoperative levels up to 6 hours postoperatively (p < 0.05). In the presence of systemic heparinization, Duroflo II heparin bondingtf the circuits has minor effects on the pattern of evolution of this inflammatory response.
Butler
John
J
Department of Cardiac Surgery, Western Infirmary, Glasgow, Scotland, United Kingdom. gilmour.wendy.wg@northglasgow.scot.nhs.uk
Murithi
Elijah W
EW
Pathi
Vivek L
VL
MacArthur
Kenneth J D
KJ
Berg
Geoffrey A
GA
D000328:Adult; D000368:Aged; D000925:Anticoagulants; D002315:Cardiopulmonary Bypass; D020099:Coated Materials, Biocompatible; D001026:Coronary Artery Bypass; D016207:Cytokines / Q000378:metabolism*; D005112:Extracorporeal Circulation; D006493:Heparin; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood*; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D016209:Interleukin-8 / Q000097:blood; D019272:Leukocyte Elastase / Q000097:blood; D008875:Middle Aged; D011659:Pulmonary Gas Exchange
D000925:Anticoagulants; D020099:Coated Materials, Biocompatible; D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D016209:Interleukin-8; D016753:Interleukin-10; D006493:Heparin; D019272:Leukocyte Elastase