OBJECTIVE: To determine the optimal model of acute respiratory distress syndrome (ARDS) using oleic acid in our laboratory and to measure the presence or absence of free radicals in this model. DESIGN: This protocol consisted of 2 phases. During the first phase, various conditions were tested, to include different doses (30 or 50 microliters) of oleic acid, different levels of support (with and without mechanical ventilation), and different injury time periods (sacrifice 4 or 8 hours after injection). During the second phase, animals were randomly assigned to experimental (injured) and control (noninjured) groups for the measurement of free radicals by nitrotyrosine Western blot and by the conversion of hydroethidine to ethidium bromide by superoxide. SETTING: Multidisciplinary laboratory and animal surgery suite. PARTICIPANTS: Twenty-seven male Sprague-Dawley rats. RESULTS: During the first phase, several animal deaths occurred in the high-dose, ventilated groups, whereas there were no deaths in the nonventilated animals. On hematoxylin and eosin stain, injury was greatest in the animals that received the higher dose of oleic acid and that were sacrificed at 8 hours. In the protocol's second phase, oxygen radical assays were negative for all experimental and control lungs. CONCLUSIONS: During this study, we successfully established a working animal model of ARDS for our laboratory. Our findings to date suggest that free radicals do not contribute to oleic acid lung injury in the early stages.
OBJECTIVE: To determine the optimal model of acute respiratory distress syndrome (ARDS) using oleic acid in our laboratory and to measure the presence or absence of free radicals in this model. DESIGN: This protocol consisted of 2 phases. During the first phase, various conditions were tested, to include different doses (30 or 50 microliters) of oleic acid, different levels of support (with and without mechanical ventilation), and different injury time periods (sacrifice 4 or 8 hours after injection). During the second phase, animals were randomly assigned to experimental (injured) and control (noninjured) groups for the measurement of free radicals by nitrotyrosine Western blot and by the conversion of hydroethidine to ethidium bromide by superoxide. SETTING: Multidisciplinary laboratory and animal surgery suite. PARTICIPANTS: Twenty-seven male Sprague-Dawley rats. RESULTS: During the first phase, several animal deaths occurred in the high-dose, ventilated groups, whereas there were no deaths in the nonventilated animals. On hematoxylin and eosin stain, injury was greatest in the animals that received the higher dose of oleic acid and that were sacrificed at 8 hours. In the protocol's second phase, oxygen radical assays were negative for all experimental and control lungs. CONCLUSIONS: During this study, we successfully established a working animal model of ARDS for our laboratory. Our findings to date suggest that free radicals do not contribute to oleic acid lung injury in the early stages.