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J Thorac Cardiovasc Surg 1996;112:1301-1306
© 1996 Mosby, Inc.

CARDIAC AND PULMONARY REPLACEMENT

Regulatory Effects of Interleukin-10 on Lung Ischemia-Reperfusion Injury

This work was supported in part by National Institutes of Health grant GM 29507 (P. A. W.). M. J. E. is supported by the United States Air Force.

Received for publication May 6, 1996; revisions requested June 26, 1996; revisions received July 12, 1996 Accepted for publication July 15, 1996. Address for reprints: G. Michael Deeb, MD, University of Michigan Hospitals, 1500 E. Medical Center Dr., 2124F Taubman Center TC/0344, Ann Arbor, MI, 48109.

Abstract

Objective: Interleukin-10, a cytokine with antiinflammatory activities, was studied to determine its effects on development of early lung reperfusion injury.Methods: Adult male rats underwent 90 minutes of left lung ischemia followed by 4 hours of reperfusion. Time-matched sham-operated control rats underwent hilar dissection but not lung ischemia. Lung injury was measured by vascular permeability to bovine serum albumin tagged with iodine 125. To evaluate the effect of exogenous interleukin-10, additional animals received interleukin-10 intravenously before ischemia. To assess the role of endogenous interleukin-10, animals received rabbit antimouse interleukin-10 immunoglobin G (or preimmune rabbit immunoglobin G) before ischemia.Results: Compared with sham control rats, ischemia-reperfusion control rats demonstrated significantly more lung injury. Animals receiving interleukin-10 had significantly less lung injury than did ischemia-reperfusion control rats. Animals receiving antiinterleukin-10 had significantly more lung injury than did animals receiving preimmune immunoglobin G. Alveolar macrophages from animals after 90 minutes of lung ischemia produced more tumor necrosis factor– in culture than did unstimulated macrophages; this production was reduced significantly by the addition of interleukin-10 to the culture medium.Conclusion: Endogenous interleukin-10 has a protective effect against early lung reperfusion injury, and interleukin-10 administration can reduce lung reperfusion injury, perhaps in part through its ability to reduce production by alveolar macrophages of tumor necrosis factor–, a known proinflammatory cytokine. (J THORAC CARDIOVASC SURG1996;112:1301-6)

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