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Ann Thorac Surg 1998;65:66-69
© 1998 The Society of Thoracic Surgeons

Original Articles: Cardiovascular

Aprotinin Enhances the Endogenous Release of Interleukin-10 After Cardiac Operations

Gary E. Hill, MD, Robert P. Diego, BS, Alfred H. Stammers, CCP, Suzanne M. Huffman, CCP, Roman Pohorecki, MD

Department of Anesthesiology, University of Nebraska Medical Center, Omaha, Nebraska, USA

Accepted for publication July 2, 1997.

Dr Hill, Department of Anesthesiology, University of Nebraska Medical Center, 600 S 42nd St, Omaha, NE 68198-4455.

Background. Cardiopulmonary bypass (CPB) is characterized by the systemic release of proinflammatory cytokines, such as tumor necrosis factor-{alpha} and the interleukins 1 and 6, as well as endogenous antiinflammatory cytokines, including interleukin-10 (IL-10). Glucocorticoids reduce tumor necrosis factor-{alpha} plasma concentrations while enhancing IL-10 plasma concentrations after CPB. Aprotinin, a serine protease inhibitor used primarily to reduce blood loss after CPB, reduces CPB-induced proinflammatory cytokine tumor necrosis factor-{alpha} release similarly to glucocorticoids. This study evaluates the effect of full-dose aprotinin on the plasma concentrations of IL-10 after CPB.

Methods. Twenty adults were randomized into a control (group C, n = 10) and a full-dose aprotinin-treated group (group A, n = 10). Plasma levels of IL-10 were measured by enzyme-linked immunosorbent assay technique at baseline (before anesthetic induction), and at 1 and 24 hours after CPB termination.

Results. A significant (p < 0.05) increase of IL-10 occurred in both groups at 1 and 24 hours after termination of CPB when compared with the same group at baseline. In group A, the increase in IL-10 was significantly greater than in group C (p < 0.05) at 24 hours after CPB.

Conclusions. These results demonstrate an endogenous antiinflammatory response generated after CPB, characterized by IL-10 release, that is enhanced by aprotinin therapy. This study demonstrates a unique antiinflammatory activity of aprotinin that may be of clinical significance.




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