Keratinocyte growth factor prevents ventilator-induced lung injury in an ex vivo rat model

Mechanical ventilation has been shown to produce lung injury characterized by noncardiogenic pulmonary edema. Keratinocyte growth factor (KGF) is a heparin-binding growth factor that causes alveolar type II pneumocyte hyperplasia. KGF pretreatment and the resultant pneumocyte hyperplasia reduce flui...

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Bibliographic Details
Published in:American journal of respiratory and critical care medicine 2000-09, Vol.162 (3), p.1081-1086
Main Authors: WELSH, David A, SUMMER, Warren R, DOBARD, Elizabeth P, NELSON, Steve, MASON, Carol M
Format: Article
Language:English
Subjects:
Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Biological and medical sciences
Capillary Permeability - drug effects
Capillary Permeability - physiology
Emergency and intensive respiratory care
Fibroblast Growth Factor 10
Fibroblast Growth Factor 7
Fibroblast Growth Factors
Growth Substances - pharmacology
Intensive care medicine
Lung - blood supply
Lung - pathology
Male
Medical sciences
Premedication
Pulmonary Edema - pathology
Pulmonary Edema - physiopathology
Pulmonary Edema - prevention & control
Rats
Rats, Sprague-Dawley
Respiration, Artificial
Respiratory Distress Syndrome, Adult - pathology
Respiratory Distress Syndrome, Adult - physiopathology
Respiratory Distress Syndrome, Adult - prevention & control
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Summary:Mechanical ventilation has been shown to produce lung injury characterized by noncardiogenic pulmonary edema. Keratinocyte growth factor (KGF) is a heparin-binding growth factor that causes alveolar type II pneumocyte hyperplasia. KGF pretreatment and the resultant pneumocyte hyperplasia reduce fluid flux in models of lung injury. We utilized the isolated perfused rat lung model to produce lung injury by varying tidal volume and the level of positive end-expiratory pressure during mechanical ventilation. Pretreatment with KGF attenuated ventilator-induced lung injury (VILI). This was demonstrated by lower wet-to-dry lung weight ratios and less lung water accumulation in the KGF group. Further, KGF prevented the decline in dynamic compliance and alveolar protein accumulation in VILI. KGF pretreatment reduced alveolar accumulation of intravascularly administered fluorescein isothiocyanate-labeled high-molecular-weight dextran. Thus, pretreatment with KFG attenuates injury in this ex vivo model of VILI via mechanisms that prevent increases in permeability.
ISSN:1073-449X
1535-4970
DOI:10.1164/ajrccm.162.3.9908099