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CARDIOVASCULAR ANESTHESIA

Activation of a Neutrophil-Derived Inflammatory Response in the Airways During Cardiopulmonary Bypass

Toru Kotani, MD^*, Yoshifumi Kotake, MD, Hiroshi Morisaki, MD, Junzo Takeda, MD, Hideyuki Shimizu, MD, Toshihiko Ueda, MD, and Akitoshi Ishizaka, MD

From the *Department of Anesthesiology, Tokyo Women's Medical University, Shinjuku, Tokyo 162-8666, Japan; and Department of Anesthesiology, Cardiovascular Surgery, and Medicine, Keio University School of Medicine, Tokyo, Japan.

Address correspondence and reprint requests to Toru Kotani, MD, Department of Anesthesiology, Tokyo Women's Medical University, 8-1, Kawadacho, Shinjuku, Tokyo 162-8666, Japan. Address e-mail to trkotani{at}aol.com.

Cardiopulmonary bypass (CPB) is believed to cause postoperative lung dysfunction. To more closely examine the inflammatory processes occurring in the airways during CPB, we serially measured inflammatory mediators, with the assistance of a new bronchoscopic microsample probe, in 11 patients undergoing repair of aortic arch aneurysms. Epithelial lining fluid (ELF) and arterial blood were sampled simultaneously after induction of anesthesia, at the time of pulmonary reperfusion, and at the end of surgery. A decrease in the Pao₂/Fio₂ ratio was observed at the end of surgery (P = 0.029). Although the ELF concentrations of interleukin (IL)-8, IL-6, and neutrophil elastase had increased significantly at the end of surgery (median = 23,200, 1818, and 12,900 µg/mL, respectively), they did not correlate with the degree of hypoxemia. Neutrophil elastase increased significantly at the time of pulmonary reperfusion, before IL-8 and IL-6, and independently of blood transfusions. At the end of surgery, IL-6 in ELF correlated with total blood transfusion volume ( = 0.731, P = 0.011). These results indicate that a neutrophil-derived inflammatory response is activated in the airway in the early phase of CPB.

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