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Am J Physiol Lung Cell Mol Physiol 264: L490-L495, 1993;
1040-0605/93 $5.00
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AJP - Lung Cellular and Molecular Physiology, Vol 264, Issue 5 490-L495, Copyright © 1993 by American Physiological Society

ARTICLES

Neutrophil-activating peptide-2 in patients with pulmonary edema from congestive heart failure or ARDS

A. B. Cohen, M. D. Stevens, E. J. Miller, M. A. Atkinson, G. Mullenbach, R. J. Maunder, T. R. Martin, J. P. Wiener-Kronish and M. A. Matthay
Department of Biochemistry, University of Texas Health Sciences Center, Tyler 75710.

We carried out studies to determine whether the neutrophil-activation peptide-2 (NAP-2) plays a role in the recruitment and/or degranulation of neutrophils into the lungs of patients with the adult respiratory distress syndrome (ARDS) or congestive heart failure (CHF). NAP-2 precursors plus NAP-2 (beta-thromboglobulin-like antigen) were measured in lung fluids and plasmas with a radioimmunoassay, and NAP-2 was separated from its precursors by high-performance liquid chromatography. Pulmonary edema fluids (PEFs) from patients with CHF contained higher concentrations of the beta-thromboglobulin-like antigen than PEFs from patients with ARDS, and bronchoalveolar lavage fluids (BALs) from patients with ARDS contained higher concentrations of beta-thromboglobulin-like antigen than BALs from normal subjects. beta-Thromboglobulin-like antigen concentration was 4.1-fold greater in PEFs from patients with CHF than in their plasmas. Chemotactically active NAP-2 was also demonstrated in PEFs but not in plasmas from patients with CHF and ARDS. These data suggest that significant platelet degranulation occurred into the lungs of the patients with CHF and that NAP-2 and other platelet constituents may contribute to fluid formation in patients with CHF.


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