OBJECTIVE: To evaluate the effects of hyperoxia exposure on lung function and the endogenous surfactant system in spontaneously breathing adult rats. DESIGN: Analysis of the pulmonary surfactant system isolated from adult rats following exposure to > 90% oxygen or room air for 48 or 72 hrs. SETTING: A basic science research laboratory in a university setting. SUBJECTS: Sixty pathogen-free Sprague-Dawley rats. INTERVENTIONS: Exposure to > 90% oxygen for 72 hrs. MEASUREMENTS AND MAIN RESULTS: Exposure to > 90% oxygen for 72 hrs resulted in significant lung dysfunction and an increase in neutrophils and total protein concentrations within the airspace compared with animals exposed to room air or 48 hrs of 90% oxygen exposure. Total alveolar surfactant and large aggregate pool sizes were increased after 72 hrs of hyperoxia compared with the other groups, and there was evidence of lipid peroxidation within these large aggregate subtractions. The biophysical function of large aggregate isolated from 72-hr hyperoxia-exposed animals was also impaired and converted into small aggregate forms faster than large aggregate from normoxia-exposed animals when assessed using in vitro surface area cycling techniques. CONCLUSIONS: Oxidative stress on the endogenous surfactant system may represent an important mechanism contributing to the surfactant dysfunction and abnormal surfactant metabolism associated with hyperoxia-induced lung injury.
OBJECTIVE: To evaluate the effects of hyperoxia exposure on lung function and the endogenous surfactant system in spontaneously breathing adult rats. DESIGN: Analysis of the pulmonary surfactant system isolated from adult rats following exposure to > 90% oxygen or room air for 48 or 72 hrs. SETTING: A basic science research laboratory in a university setting. SUBJECTS: Sixty pathogen-free Sprague-Dawley rats. INTERVENTIONS: Exposure to > 90% oxygen for 72 hrs. MEASUREMENTS AND MAIN RESULTS: Exposure to > 90% oxygen for 72 hrs resulted in significant lung dysfunction and an increase in neutrophils and total protein concentrations within the airspace compared with animals exposed to room air or 48 hrs of 90% oxygen exposure. Total alveolar surfactant and large aggregate pool sizes were increased after 72 hrs of hyperoxia compared with the other groups, and there was evidence of lipid peroxidation within these large aggregate subtractions. The biophysical function of large aggregate isolated from 72-hr hyperoxia-exposed animals was also impaired and converted into small aggregate forms faster than large aggregate from normoxia-exposed animals when assessed using in vitro surface area cycling techniques. CONCLUSIONS: Oxidative stress on the endogenous surfactant system may represent an important mechanism contributing to the surfactant dysfunction and abnormal surfactant metabolism associated with hyperoxia-induced lung injury.
Authors: Ava M Puccio; Leslie A Hoffman; Hülya Bayir; Thomas G Zullo; Michael Fischer; Joseph Darby; Sheila Alexander; C Edward Dixon; David O Okonkwo; Patrick M Kochanek Journal: J Neurotrauma Date: 2009-08 Impact factor: 5.269
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Authors: Sebastian Hafner; François Beloncle; Andreas Koch; Peter Radermacher; Pierre Asfar Journal: Ann Intensive Care Date: 2015-11-19 Impact factor: 6.925