Toxicology of blast over-pressure
Toxicology of blast over-pressure
复制标题
DOI：
10.1016/s0300-483x(97)03651-2
复制
发表时间：
1997-07-25
期刊：
影响因子：
4.5
通讯作者：
Elsayed, NM
中科院分区：
文献类型：
--
作者：
Elsayed, NM
爆炸超压（BOP）或高能脉冲噪声，是由炸药爆炸或武器发射引起的环境大气压力瞬间急剧上升。曾经局限于军事场所的爆炸，以及在较小程度上局限于职业场所的爆炸，正变得越来越普遍，因为平民人口现在越来越有可能受到世界范围内越来越频繁发生的恐怖主义爆炸所造成的防喷器污染。暴露于入射防喷器波会造成听觉和非听觉损伤。防喷器损伤的主要目标是中空器官、耳、肺和胃肠道。此外，心脏、脾脏和大脑等实体器官也会受到损伤。然而，肺对损伤更敏感，它的损伤可能导致死亡。损伤的病理生理反应和死亡率已经得到了广泛的研究，但对损伤的生化表现和分子机制却很少关注。防喷器造成的损伤通常是由于其对机体的外部物理冲击造成内部机械损伤。然而，根据里德陆军研究所呼吸研究部门和匹兹堡大学职业健康部门进行的实验，提出了一个新的假设。这一假设表明，微妙的生化变化，即自由基介导的氧化应激发生，并有助于bop诱导的损伤。了解这些变化的病因可能会揭示损伤的分子机制，并可能提供新的治疗策略。在本次研讨会上，讨论了防喷器损伤的听觉、非听觉、生理、病理行为和生化表现，以及防喷器损伤的预测建模和目前的治疗方式。(C) 1997爱思唯尔科学爱尔兰有限公司
Blast overpressure (BOP) or high energy impulse noise, is the sharp instantaneous rise in ambient atmospheric pressure resulting from explosive detonation or firing of weapons. Blasts that were once confined to military and to a lesser extent, occupational settings, are becoming more universal as the civilian population is now increasingly at risk of exposure to BOP from terrorist bombings that are occurring worldwide with greater frequency. Exposure to incident BOP waves can cause auditory and non-auditory damage. The primary targets for BOP damage are the hollow organs, ear, lung and gastrointestinal tract. In addition, solid organs such as heart, spleen and brain can also be injured upon exposure. However, the lung is more sensitive to damage and its injury can lead to death. The pathophysiological responses, and mortality have been extensively studied, but little attention, was given to the biochemical manifestations, and molecular mechanism(s) of injury. The injury from BOP has been, generally, attributed to its external physical impact on the body causing internal mechanical damage. However, a new hypothesis has been proposed based on experiments conducted in the Department of Respiratory Research, Waiter Reed Army Institute of Research, and later in the Department of Occupational Health, University of Pittsburgh. This hypothesis suggests that subtle biochemical changes namely, free radical-mediated oxidative stress occur and contribute to BOP-induced injury. Understanding the etiology of these changes may shed new light on the molecular mechanism(s) of injury, and can potentially offer new strategies for treatment. In this symposium, BOP research involving auditory, non-auditory, physiological, pathological behavioral, and biochemical manifestations as well as predictive modeling and current treatment modalities of BOP-induced injury are discussed. (C) 1997 Elsevier Science Ireland Ltd.