IngentaConnect Liver-type fatty acid binding protein in serum and broncho-alveol...

Authors: Lachmann, R. A.¹; Werchan, S.¹; Schachtrup, C.²; Haitsma, J. J.¹; Spener, F.²; Lachmann, B.¹

Source: Clinical Physiology and Functional Imaging, Volume 26, Number 6, November 2006 , pp. 371-375(5)

Abstract:

Summary Introduction

Liver-type fatty acid binding proteins (L-FABP) have been shown to be present in alveolar macrophages and type II pneumocytes of the lung. This study determined levels of L-FABP in serum and broncho-alveolar lavage (BAL) during experimental acute respiratory failure (ARF) to evaluate whether this molecule can serve as a marker for lung damage. Methods

Male Sprague-Dawley rats (n = 24) were ventilated and either lung lavaged or lavaged and treated with surfactant, and compared to ventilated, non-lavaged controls. Blood samples were drawn every hour for 4 h to measure L-FABP concentrations in serum. At the end of the experiment a BAL was performed to determine L-FABP levels in BAL fluid. L-FABP was measured with a sandwich enzyme-linked immunosorbent assays. Results

Serum L-FABP concentrations rose significantly during the first 2 h of ventilation in all groups compared with baseline values. After 2 h L-FABP levels were significantly higher in lavaged animals compared with the ventilated controls and to animals treated with surfactant. After 4 h of ventilation, L-FABP in BAL was significantly higher in lavaged, non-surfactant treated animals compared with the ventilated controls. Conclusion

In the early phase of experimental ARF serum L-FABP levels correlate well with the degree of lung injury.

Keywords: alveolar macrophages; mechanical ventilation; rat; surfactant; type II pneumocytes

Document Type: Research article

DOI: 10.1111/j.1475-097X.2006.00703.x

Affiliations: 1: Department of Anesthesiology, Erasmus MC-Faculty, Rotterdam, The Netherlands 2: Department of Biochemistry, University of Münster, Münster, Germany

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Liver-type fatty acid binding protein in serum and broncho-alveolar lavage in a model of acute respiratory failure because of surfactant depletion - a possible marker for lung damage?