Elsayed N M, Gorbunov N V, Kagan V E
Department of Respiratory Research, Walter Reed Army Institute of Research, Washington, DC 20307, USA.
Toxicology. 1997 Jul 25;121(1):81-90. doi: 10.1016/s0300-483x(97)03657-3.
Blast overpressure (BOP) is the abrupt, rapid, rise in atmospheric pressure resulting from explosive detonation, firing of large-caliber weapons, and accidental occupational explosions. Exposure to incident BOP waves causes internal injuries, mostly to the hollow organs, particularly the ears, lungs and gastrointestinal tract. BOP-induced injury used to be considered of military concern because it occurred mostly in military environments during military actions or training, and to a lesser extent during civilian occupational accidents. However, in recent years with the proliferation of indiscriminate terrorist bombings worldwide involving civilians, blast injury has become a societal concern, and the need to understand the biochemical and molecular mechanism(s) of injury, and to find new and effective methods for treatment gained importance. In general, past BOP research has focused on the physiological and pathological manifestations of incapacitation, thresholds of safety, and on predictive modeling. However, we have been studying the molecular mechanism of BOP-induced injury, and recently began to have an insight into that mechanism, and recognize the role of hemoglobin released during hemorrhage in catalyzing free radical reactions leading to oxidative stress. In this report we discuss the biochemical changes observed after BOP exposure in rat blood and lung tissue, and propose a biochemical mechanism for free radical-induced oxidative stress that can potentially complicate the injury. Moreover, we observed that some antioxidants can interact with Hb oxidation products (oxy-, met- and oxoferrylHb) and act as prooxidants that can increase the damage rather than decrease it.
爆炸超压（BOP）是由炸药爆炸、大口径武器射击及意外职业爆炸导致的大气压力突然、迅速升高。暴露于突发BOP波会导致内伤，主要是中空器官受损，尤其是耳朵、肺部和胃肠道。BOP所致损伤过去被认为主要与军事相关，因为它大多发生在军事行动或训练期间的军事环境中，在民用职业事故中发生的程度相对较小。然而，近年来，随着全球范围内涉及平民的滥杀滥伤恐怖爆炸事件激增，爆炸伤已成为一个社会问题，了解损伤的生化和分子机制以及寻找新的有效治疗方法变得至关重要。总体而言，过去对BOP的研究主要集中在失能的生理和病理表现、安全阈值以及预测模型方面。然而，我们一直在研究BOP所致损伤的分子机制，最近开始深入了解该机制，并认识到出血期间释放的血红蛋白在催化自由基反应导致氧化应激中所起的作用。在本报告中，我们讨论了在大鼠血液和肺组织中BOP暴露后观察到的生化变化，并提出了一种自由基诱导氧化应激的生化机制，这种氧化应激可能会使损伤复杂化。此外，我们观察到一些抗氧化剂可与血红蛋白氧化产物（氧合血红蛋白、高铁血红蛋白和氧合高铁血红蛋白）相互作用，并作为促氧化剂发挥作用，从而增加而非减少损伤。
