BACKGROUND: A critical immediate determinant of survival after exposure to blast overpressure (BOP) is pulmonary damage, but mechanisms of injury and the course of recovery are not well understood. The objective of this study was to characterize the progression of oxidative and inflammatory responses in lungs as well as the activation of consequent protective mechanisms after exposure to medium intensity BOP. METHODS: Rats were exposed to a moderate (approximately 120 kPa) level of BOP in a pneumatically driven shock tube. At different times (2-192 hours) after exposure, lungs were examined for pathologic signs of injury, markers of inflammatory responses, and indicators of oxidative and nitrative damage. RESULTS: The results showed a postblast activation of inflammatory response (increase of myeloperoxidase activity, CINC-1, ICAM-1, and iNOS), increase in protein oxidation and nitration, and development of gross diffused hemorrhage in lungs. The initial phase of lung damage that peaked at 24 to 48 hours after exposure to BOP was followed by gradual dissolution of inflammation and oxidation that were complete by 192 hours. Resolution of morphologic damage and inflammation in lungs concurred with activation of expression of antioxidant enzymes heme oxygenase-1 (HO-1) and manganese superoxide dismutase (MnSOD). Plasma level of gelsolin, a marker of acute lung damage was decreased at 24 hours postblast and later returned to the control level. CONCLUSIONS: The study shows the role of adaptive anti-oxidant and anti- inflammatory mechanisms in lung recovery after injury caused by exposure to BOP.
BACKGROUND: A critical immediate determinant of survival after exposure to blast overpressure (BOP) is pulmonary damage, but mechanisms of injury and the course of recovery are not well understood. The objective of this study was to characterize the progression of oxidative and inflammatory responses in lungs as well as the activation of consequent protective mechanisms after exposure to medium intensity BOP. METHODS:Rats were exposed to a moderate (approximately 120 kPa) level of BOP in a pneumatically driven shock tube. At different times (2-192 hours) after exposure, lungs were examined for pathologic signs of injury, markers of inflammatory responses, and indicators of oxidative and nitrative damage. RESULTS: The results showed a postblast activation of inflammatory response (increase of myeloperoxidase activity, CINC-1, ICAM-1, and iNOS), increase in protein oxidation and nitration, and development of gross diffused hemorrhage in lungs. The initial phase of lung damage that peaked at 24 to 48 hours after exposure to BOP was followed by gradual dissolution of inflammation and oxidation that were complete by 192 hours. Resolution of morphologic damage and inflammation in lungs concurred with activation of expression of antioxidant enzymes heme oxygenase-1 (HO-1) and manganese superoxide dismutase (MnSOD). Plasma level of gelsolin, a marker of acute lung damage was decreased at 24 hours postblast and later returned to the control level. CONCLUSIONS: The study shows the role of adaptive anti-oxidant and anti- inflammatory mechanisms in lung recovery after injury caused by exposure to BOP.
Authors: D Kacy Cullen; Kevin D Browne; Yongan Xu; Saleena Adeeb; John A Wolf; Richard M McCarron; Shu Yang; Mikulas Chavko; Douglas H Smith Journal: J Neurotrauma Date: 2011-11 Impact factor: 5.269
Authors: Ryan D Readnower; Mikulas Chavko; Saleena Adeeb; Michael D Conroy; James R Pauly; Richard M McCarron; Patrick G Sullivan Journal: J Neurosci Res Date: 2010-09-29 Impact factor: 4.164
Authors: Dexter V Reneer; Richard D Hisel; Joshua M Hoffman; Richard J Kryscio; Braden T Lusk; James W Geddes Journal: J Neurotrauma Date: 2011-01 Impact factor: 5.269