Lung injury and recovery after exposure to blast overpressure
Lung injury and recovery after exposure to blast overpressure
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DOI：
10.1097/01.ta.0000233742.75450.47
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发表时间：
2006-10-01
影响因子：
--
通讯作者：
McCarron, Richard M.
中科院分区：
文献类型：
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作者：
Chavko, Mikulas;Prusaczyk, W. Keith;McCarron, Richard M.
背景：暴露于爆炸超压（BOP）后存活的一个关键直接决定因素是肺损伤，但损伤机制和恢复过程尚不清楚。本研究的目的是表征暴露于中等强度bop后肺部氧化和炎症反应的进展以及随之而来的保护机制的激活。大鼠在气压驱动的冲击管中暴露于中等（类似于120 kPa）水平的防喷器。在暴露后的不同时间（2-192小时），检测肺部损伤的病理体征、炎症反应标志物以及氧化和硝化损伤指标。结果：细胞后炎症反应激活（髓过氧化物酶活性、cinc1、ICAM-1和NOS增加），蛋白质氧化和硝化增加，肺部弥漫性大出血发生。肺损伤的初始阶段在接触防喷器后24至48小时达到顶峰，随后炎症和氧化逐渐溶解，并在192小时完成。肺部形态学损伤和炎症的消退与抗氧化酶血红素氧化酶-1 （HO-1）和锰超氧化物歧化酶（MnSOD）表达的激活同时发生。急性肺损伤标志物明胶蛋白水平在心肌梗死后24小时下降，随后恢复到对照组水平。该研究显示适应性抗氧化和抗炎机制在BOP损伤后肺恢复中的作用。
Backround: 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 (similar to 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 NOS), 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.