Evidence for inflammatory responses of the lungs during coronary artery bypass grafting with cardiopulmonary bypass

Objective: The occurrence of a systemic inflammatory reaction during cardia c surgery with cardiopulmonary bypass (CPB) has been well established, and the heart itself has been shown to release inflammatory mediators after isc hemia. The hypothesis of the present study was that the lungs are also a si te of inflammatory responses during early reperfusion. Methods: In 20 consecutive patients undergoing coronary artery bypass graft ing, blood was simultaneously drawn from the right atrium (RA) and the pulm onary vein (PV) before CPB and at 1 min, 10 min, and 20 min of reperfusion. The levels of interleukin (1L)-6, IL-8, IL-10, and tumor necrosis factor ( TNF)-alpha were determined, as well as the adhesion molecules CD41 and CD62 on platelets and CD11b and CD41 on leukocytes. As a measure of the pulmona ry release, ratios of PV and RA levels were calculated. Results: Before CPB, the concentrations of cytokines tended to be lower in the PV compared with the RA. At 1 min of reperfusion, no significant concen tration increases were found in the PV. At 10 min of reperfusion, the PV/RA ratio (mean +/- SEM) for IL-6 was 2.06 +/- 0.37 and 1.24 +/- 0.15 for IL-8 (p = 0.02 and p = 0.04, respectively, compared with the pre-CPB ratios of 0.89 +/- 0.4 and 0.99 +/- 0.2). At 20 min of reperfusion, PV/RA ratios for IL-6 (1.95 +/- 0.37) and IL-10 (0.99 +/- 0.4) were higher than before CPB ( 0.89 +/- 0.04, p = 0.05 and 0.85 +/- 0.06, p = 0.03, respectively). Adhesio n molecule counts on platelets and polymorphonuclear neutrophils (PMNs) ten ded to be higher in the PV than in the RA before CPB. At 1 min of reperfusi on, the PV/RA ratio of CD41 on monocytes (0.89 +/- 0.04) and of CD41 on PMN s (1.05 +/- 0.05) was less than before CPB (1.24 +/- 0.08, p = 0.0002 and 1 .55 +/- 0.14, p = 0.0002). At 10 min and 20 min of reperfusion, similar cha nges were found. Conclusions: The observed changes indicate an inflammatory response of the lungs. Proinflammatory cytokines are increased in pulmonary venous blood. A t the same time, activated blood cells are retained in the pulmonary circul ation. This may contribute to pulmonary dysfunction almost routinely observ ed after CPB.