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Ann Thorac Surg 2001;71:1825-1832
© 2001 The Society of Thoracic Surgeons
a Department of Biochemistry, The University of Texas Health Center at Tyler, Tyler, Texas, USA
b Vivarium, The University of Texas Health Center at Tyler, Tyler, Texas, USA
c Medical Research Service of the Seattle Veterans Affairs Medical Center, and the Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Washington School of Medicine, Seattle, Washington, USA
d Department of Thoracic and Cardiovascular Surgery, Saga Medical School, Saga, Japan
Accepted for publication January 24, 2001.
Address reprint requests to Dr Miller, Department of Biochemistry, The University of Texas Health Center at Tyler, 11937 US Highway 271, Tyler, TX 75708–3154
e-mail: ed.miller{at}uthct.edu
Background. The aim of this study is to determine the relationships between the cytokines and the inflammatory response in reexpansion pulmonary edema (RPE).
Methods. We examined the cell population, epithelial permeability measured by Evans blue dye (EB), ßglucuronidase and cytokine concentrations in bronchoalveolar lavage fluid (BALF) and/or blood using a rabbit RPE model.
Results. We confirmed that RPE is characterized by recruitment of polymorphonuclear leukocytes (PMNs), the release of PMN granular contents into the air spaces, and increased vascular permeability. These findings were highly correlated with increased interleukin-8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) concentrations in the BALF. Growth related oncogene (GRO) was detected in the BALF from only 2 of the 7 reexpanded lungs while TNF
was not detected in any rabbits. A similar but less severe inflammatory response to the reexpanded lung was found in the contralateral lung.
Conclusions. IL-8 and MCP-1 may play important roles in the development of RPE; the inflammatory response is independent of TNF and unilateral reexpansion of the lung induces an inflammatory response not only in the reexpanded lung but also in the contralateral lung.
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