HYPOTHERMIA DURING CARDIOPULMONARY BYPASS DELAYS BUT DOES NOT PREVENTNEUTROPHIL-ENDOTHELIAL CELL-ADHESION - A CLINICAL-STUDY

Background An accurate evaluation of warm heart surgery cannot be limi ted to the assessment of the myocardial effects of warm blood cardiopl egia but should also address the effects of systemic normothermia on t he inflammatory response to cardiopulmonary bypass. A major component of this response is the endothelial adhesion of neutrophils, because i t is linked to the release of cytotoxic compounds. This study was desi gned (1) to characterize the bypass-induced changes in the expression of neutrophil adhesion molecules (L-selectin and beta(2)-integrins) an d (2) to assess the influence of bypass temperature on these changes. Methods and Results Twenty case-matched patients undergoing open-heart procedures were divided into two equal groups according to the core t emperature during cardiopulmonary bypass: warm (33.4+/-0.3 degrees C) or cold (27.1+/-0.4 degrees C, P<.0001 versus warm). Arterial blood sa mples were collected before, during, and 30 minutes after bypass and p rocessed for the expression of L-selectin and beta(2)-integrins (CD11a , CD11b, and CD11c) with flow cytometry. Warm bypass was associated wi th an early and sustained upregulation of CD11b. In contrast, hypother mia resulted in a strikingly less pronounced CD11b upregulation during bypass. However, CD11b expression sharply increased thereafter so tha t 30 minutes after bypass, it was no longer significantly different be tween the two groups. Changes in CD11c expression grossly paralleled t hose described for CD11b. Neither CD11a nor L-selectin changed signifi cantly from baseline values in either group. Conclusions Clinical card iopulmonary bypass is associated with a marked upregulation of the neu trophil CD11b and CD11c integrins. Hypothermia delays but does not pre vent the increased expression of these adhesion molecules, which could consequently represent logical targets for interventions designed to blunt the neutrophil-mediated component of bypass-induced inflammatory tissue damage.