Extracorporeal circulation does not induce intra-alveolar release of Endothelin 1, but only a modest overproduction in pulmonary circulation

Objective. To investigate whether ECC may produce regional Liberation of in flammatory mediators capable of inducing vascular effects and organ damage. Experimental design: randomized, comparative study. Setting: cardiac surge ry department in a University hospital. Patients: fifteen patients undergoi ng coronary artery bypass grafting (CABG, group A) and ten patients operate d for infrarenal abdominal aortic aneurysm (controls, group B) have been st udied. Measures: levels of Interleukin 1 beta (IL1), Tumor Necrosis Factor alpha (TNF), Interleukin 6 (IL6), and Endothelin 1 (ET1) were measured in p ulmonary capillary, arterial, and venous blood and in bronchoalveolar lavag es (BAL) before, during and after extracorporeal circulation (ECC) or surgi cal intervention. Results. TNF-alpha (never >35 pg/ml) and IL1 beta (range 20-300 pg/ml) valu es did not change over time for both groups, IL6 concentrations in all samp les of group A increased between five and twenty fold, during and after ECC (from 3-5 pg/ml up to 240 pg/ml, p<0.001). This trend was similar in contr ols after surgical stress. Endothelin 1 was always undetectable in the BAC fluid, with a modest, but significant increase in pulmonary capillary blood of group A, after ECC, (from 11+/-4 pg/ml to 18+/-5 pg/ml, p<0.001). This increment correlated well with the PVR increase, but was transient and afte r 24 hours, ET1 values returned to baseline levels. Mean values of ET1 incr eased also in controls, but not significantly. Conclusions. ECC may induce ET1 liberation in pulmonary circulation with tr ansient pulmonary vasoconstriction, but wihout intra-alveolar release, or l ung damage. Augmented concentrations of IL6 probably express a response to surgical procedure rather than an effect exclusively related to ECC.