INFLUENCE OF TEMPERATURE ON NEUTROPHIL TRAFFICKING DURING CLINICAL CARDIOPULMONARY BYPASS

Background The adhesion of neutrophils to endothelial cells and their subsequent transendothelial migration play a major role in inflammator y damage elicited by cardiopulmonary bypass (CPB) because these events are linked to the release of cytotoxic proteases and oxidants. Howeve r, the patterns of neutrophil trafficking in relation to systemic temp erature during clinical CPB have not yet been characterized. Methods a nd Results Twenty case-matched patients undergoing warm (31.8+/-0.4 de grees C) or cold (26.3+/-0.5 degrees C, P<.0001 versus warm) bypass we re studied. Blood samples were simultaneously collected from the right and left atria before, at the end of, and 30 minutes after CPB. Plasm a levels of C3a, P- and E-selectins, elastase, and interleukin-8 were determined by immunoassays. The results demonstrate: (1) a rise in C3a , reflecting complement activation, (2) a fall in soluble E-selectin c onsistent with an increased adhesiveness of activated neutrophils, (3) a rise in soluble P-selectin expected to enhance endothelial adhesion of these neutrophils, (4) a rise in elastase, suggesting an adhesion- triggered neutrophil degranulation, and finally (5) a rise in interleu kin-8 that is likely to promote transendothelial migration of adherent neutrophils. All of these changes occurred in the two groups of patie nts and were significant compared with prebypass values. However, in n one of the groups was there a significant difference between right and left atrial values for any of the markers. The single difference betw een cold and warm bypass patients was a significant reduction of elast ase release in the cold group (P<.001 versus the warm group). Conclusi ons Clinical CPB is associated with biological changes suggesting the occurrence of neutrophil trafficking. Hypothermia provides only partia l protection through a reduced release of elastase. Overall, these res ults reinforce the rationale for the development of therapeutic strate gies targeted at blunting the neutrophil-mediated component of bypass- induced inflammatory damage.