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Keratinocyte growth factor prevents intra-alveolar oedema in experimental lung isografts

¹ Laboratory of Experimental Surgery, Dept of General and Thoracic Surgery, ² Dept of Internal Medicine, University of Giessen Lung Center, Justus-Liebig-University Giessen, Giessen, ³ Clinical Research Group "Chronic Airway Diseases", Clinic of Internal Medicine (Respiratory Medicine), Philipps University of Marburg, Marburg, and ⁴ Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover, Germany. ⁵ These authors contributed equally to the study.

CORRESPONDENCE: V. Grau, Laboratory of Experimental Surgery, Dept of General and Thoracic Surgery, University of Giessen Lung Center, Justus-Liebig-University Giessen, Rudolf-Buchheim-Str. 7, D-35385 Giessen, Germany. Fax: 49 6419944709. E-mail: Veronika.Grau{at}chiru.med.uni-giessen.de

Keywords: Keratinocyte growth factor, lung, oedema, primary graft dysfunction, transplantation

Received: January 31, 2007
Accepted September 13, 2007

Primary graft dysfunction, characterised by intra-alveolar oedema, is a major obstacle in pulmonary transplantation. The present study evaluates the potential of keratinocyte growth factor (palmiferin; N23-KGF) for the prevention of oedema in lung transplants.

Intratracheal instillation of 5 mg·kg^–1 N23-KGF was performed in Lewis rats on days 3 and 2 before explantation. Control animals obtained an equivalent volume of vehicle. Left lungs were isogeneically transplanted and the graft recipients were sacrificed 1 day later for stereological analysis of intra-alveolar oedema and bronchoalveolar lavage. The total protein and phospholipid content, as well as surfactant proteins, were measured. Surfactant activity was analysed with a pulsating bubble surfactometer.

In grafts from control treated donors, the fraction of intra-alveolar oedema amounted to 3.4±1.1% of the total parenchymal volume. Treatment of donor lungs with N23-KGF reduced oedema to a fraction of 1.6±0.8%. In the lavage fluid of pulmonary grafts from N23-KGF-treated donors, the total protein content was decreased compared with vehicle-treated lung transplants, whereas phospholipids did not differ. The protein fraction contained increased amounts of surfactant protein-C after N23-KGF treatment and surfactant function was improved.

Treatment of donor lungs with palifermin protects against intra-alveolar oedema formation upon transplantation. This effect appears to be mediated by an improved surfactant homeostasis.

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