Cytokine mediated endothelial activation during and after normothermic cardiopulmonary bypass: heparin-bonded versus non heparin-bonded circuits.

Abstract

Studies evaluating cytokine production under normothermic cardiopulmonary bypass (CPB) are limited. We evaluated cytokine production, levels of thrombomodulin (TM), and soluble endothelium-derived adhesion molecules (ICAM-1) under normothermic CPB with and without heparin-bonded circuits. Nine patients treated with non heparin-bonded circuits (control group), and seven patients treated with heparin-bonded circuits (heparin group) were the subjects. Granulocyte elastase (G-E), and interleukin (IL) -6 and IL-8 were chosen as proinflammatory mediators, and TM and ICAM-1 served as indicators for endothelial damage. Blood samples were obtained before CPB, 30 minutes after initiation of CPB, at the termination of CPB, and 2 and 24 hours after CPB. G-E values in the heparin group were lower than those in the control group after 30 minutes of CPB. A G-E surge occurred at the end of CPB, and IL-6 and IL-8 surges were observed 2 hours after CPB in both groups. TM and ICAM-1 values, which were reduced at the initiation of CPB, returned to initial levels 2 hours after CPB, and exceeded them 24 hours after CPB compared with preCPB levels. Both groups showed similar changes. We conclude that there are no significant differences in serial G-E, IL-6, IL-8, TM, or ICAM-1 levels between the heparin and control groups during or after normothermic CPB for 2 to 3 hours.