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CARDIOVASCULAR ANESTHESIA

Cardiopulmonary Bypass Produces Greater Pulmonary than Systemic Proinflammatory Cytokines

Naoki Kotani, MD^*, Hiroshi Hashimoto, MD^*, Daniel I. Sessler, MD, Masatoshi Muraoka, MD^*, Jian-Sheng Wang, MD, Michael F. O’Connor, MD, and Akitomo Matsuki, MD^*

*Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki, Japan; Department of Anesthesia and Perioperative Care, University of California–San Francisco, San Francisco, California; and Department of Anesthesia and Critical Care, University of Chicago, Chicago, Illinois

Address correspondence and reprint requests to Naoki Kotani, MD, Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki 036-8562, Japan. Address e-mail to nao{at}cc.hirosaki-u.ac.jp

Cardiopulmonary bypass (CPB) impairs pulmonary endothelial injury in part by increasing expression of adhesion molecules that results in neutrophil influx. Although numerous proinflammatory cytokines up-regulate these responses, the extent to which systemic and pulmonary proinflammatory cytokines increase remains unknown. We therefore examined systemic and pulmonary gene expression and production of proinflammatory cytokines during CPB. Bronchoalveolar lavage and peripheral blood sampling were performed just after the induction of anesthesia and at the end of surgery in 80 patients undergoing CPB. RNA was extracted from harvested cells and cDNA was synthesized by reverse transcription. The expression of interleukin (IL)-6, IL-8, and tumor necrosis factor- (TNF-) was measured by semiquantitative polymerase chain reaction using ß-actin as an internal standard. We also measured these cytokines in cultured alveolar macrophages and plasma monocytes in standard medium alone, or in the presence of lipopolysaccharide. We found 2- to 20-fold increases in gene expression for these cytokines in both plasma and alveolar leukocytes at the end of surgery. However, the increases were 4–8 times greater in alveolar than plasma leukocytes. Alveolar macrophages obtained at the end of surgery produced 1.5–3 times more IL-6, IL-8, and TNF- than those obtained at the beginning (P < 0.0001). Although plasma monocytes produced more IL-8 at the end of surgery (P < 0.001), TNF- and IL-6 did not increase. The production of all cytokines was 1.5–3 times greater in alveolar macrophages obtained at the end of surgery than in plasma monocytes obtained simultaneously (P < 0.005). Our data thus suggest that CPB provokes a greater pulmonary than systemic inflammatory response.

Implications: Both gene expression and production of proinflammatory cytokines were greater in alveolar than plasma leukocytes after cardiopulmonary bypass. These results suggest that cardiopulmonary bypass provokes more serious pulmonary than systemic inflammatory responses.

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