Januszkiewicz A J, Mundie T G, Dodd K T
Walter Reed Army Institute of Research, Department of Respiratory Research, Washington, D.C. 20307-5100, USA.
Toxicology. 1997 Jul 25;121(1):51-63. doi: 10.1016/s0300-483x(97)03655-x.
Lung contusion has been identified as a primary blast injury. These experiments addressed a fundamental and overt endpoint of primary blast injury, incapacitation (performance decrement). Respiration, hemodynamics, and blood gases were measured in sheep undergoing incremental exercise challenge before and 1 h after simulated blast exposure of the thorax. Pathologic examination of lung tissue was performed after exposure and exercise testing. Blast overpressure was simulated in the laboratory using a compressed air-driven shock tube. Three levels of lung injury (Levels 1-3, 'Trivial', 'Slight', and 'Moderate' injury, respectively) were examined for effects on maximal oxygen consumption (VO[2max]), an index of cardiorespiratory fitness. Resting hemodynamics and blood gases were relatively normal an hour after exposure, immediately before exercise. However, Levels 1-3 lung injury were associated with average 4.8, 29.9 and 49.3% VO(2max). decreases, respectively. These performance decrements for Levels 2 and 3 were significantly different from respective controls (non-exposed). Exercise caused significant hemoconcentration in sheep under control conditions, before exposure (resting 9.5 +/- 0.9, end-exercise 11.8 +/- 0.9 g/100 ml). Blast exposure resulted in average decreases of 4.9 +/- 3.4, 12.8 +/- 4.0, and 12.6 +/- 3.3% in exercise-induced hemoconcentration for Levels 1-3 injury, respectively. Normal exercise-induced hemodynamic increases were also attenuated after exposure. Levels 2 and 3 injury resulted in average 22.6 +/- 2.9 and 18.5 +/- 11.2% stroke volume decreases, and also 22.3 +/- 8.4 and 29.0 +/- 14.2% cardiac output decreases, respectively, during exercise. While blast lung pathology and pulmonary function changes could account for post-blast performance decrements, these experiments suggest that in sheep, early after exposure, diminished hemoconcentration and cardiac disfunction may also contribute to decreased exercise performance.
肺挫伤已被确认为主要的爆震伤。这些实验针对主要爆震伤的一个基本且明显的终点——失能(性能下降)展开研究。在对绵羊胸部进行模拟爆震暴露前及暴露后1小时,对其进行递增运动挑战,并测量呼吸、血流动力学和血气指标。在暴露和运动测试后,对肺组织进行病理检查。在实验室中使用压缩空气驱动的激波管模拟爆震超压。研究了三种肺损伤程度(分别为1 - 3级,即“轻微”“轻度”和“中度”损伤)对最大耗氧量(VO₂max)的影响,VO₂max是心肺适能的一个指标。暴露后1小时,即运动前,静息血流动力学和血气指标相对正常。然而,1 - 3级肺损伤分别导致VO₂max平均下降4.8%、29.9%和49.3%。2级和3级损伤导致的性能下降与各自的对照组(未暴露组)相比有显著差异。在暴露前的对照条件下,运动使绵羊出现显著的血液浓缩(静息时为9.5±0.9,运动结束时为11.8±0.9 g/100 ml)。爆震暴露导致1 - 3级损伤的运动诱导血液浓缩平均分别下降4.9±3.4%、12.8±4.0%和12.6±3.3%。暴露后,正常运动诱导的血流动力学增加也减弱了。2级和3级损伤在运动期间分别导致平均每搏输出量下降22.6±2.9%和18.5±11.2%,心输出量下降22.3±8.4%和29.0±14.2%。虽然爆震性肺病理和肺功能变化可以解释爆震后性能下降的原因,但这些实验表明,在绵羊中,暴露后早期,血液浓缩减弱和心脏功能障碍也可能导致运动性能下降。