冲击伤对大鼠学习和记忆的影响

实验用Wistar大鼠30只,分为冲击波全身致伤组(Ⅰ组),冲击波头部致伤组(Ⅱ组)和对照组三组,用自行研制的BST系列生物激波管产生的冲击波致伤,分别以大鼠穿梭箱主动回避反应习得率和消退率作为学习和记忆的指标,观察冲击伤对学习和记忆功能     

肺冲击伤实验与检测方法研究进展

肺是冲击波作用于人体时易于受伤的靶器官之一.肺冲击伤在战时和平时意外爆炸事故中较多见,是军事医学和灾害医学中的重要研究课题之一.肺受冲击波致伤后会引起机体生理、病理、生化方面的改变,引发肺部炎性反应和细胞凋亡,并激活TNF-α、IL-6、IL-8、IL-1β等细胞炎性因子,最终导致急性呼吸窘迫综合征(ARDS).介绍了肺冲击伤的衍生过程和损伤特点,以及实验室模拟肺冲击伤的4种常用致伤装置即生物激波管、分段冲击波发生器、微型冲击波发生器、激光调控应力波发生器；此外,还列举了肺冲击伤的评分标准、病理和生化的检测指标.旨在为肺冲击伤实验动物的建模提供参考.     

幼兔重度肺冲击伤动物模型的建立

目的建立稳定的幼兔重度肺冲击伤实验动物模型,为未成熟肺冲击伤机制和肺损伤救治研究提供理想的动物模型。方法致伤驱动压初筛:选取4周龄新西兰白兔16只,随机分为驱动压4.0 MPa组和4.5 MPa组,采用BST-Ⅰ型生物激波管,以相应的驱动压力致伤,对比2组肺冲击伤伤情。肺冲击伤伤情特点观察:选取4周龄新西兰白兔48只,随机分为正常对照组(8只)和冲击伤组(40只),依前面研究结果,冲击伤组采用4.5 MPa驱动压进行致伤;分别于伤即刻(0 h)、2 h、4 h、6 h、12 h、24 h、48 h及72 h观测动物生命体征和生理指标、肺大体解剖和光镜病理、测定肺组织含水量等。结果致伤驱动压初筛:2组动物均存活,4.0 MPa组冲击波超压为(328.16±4.78)kP a,重度肺冲击伤率为12.5%,AIS评分(3.38±0.52)分;4.5 MPa组冲击波超压为(395.04±11.74)kP a,重度肺冲击伤率为87.5%,AIS评分(4.13±0.64)分。肺冲击伤伤情特点观察:致伤动物均存活,伤后即刻出现持续约0.5 h的精神萎靡等情况,随后动物呼吸和心率等加快,肺出现广泛片状出血和水肿,肺含水量显著增加,多为重度冲击伤,AIS评分(3.98±0.55)分,肺光镜病理以肺组织断裂、出血、水肿,伴炎细胞浸润为主。结论利用BST-Ⅰ型生物激波管,采用4.5 MPa驱动压可建立稳定的4周龄新西兰白兔重度冲击伤模型,此模型伤情稳定,可用于未成熟肺冲击伤机制和肺损伤救治的实验研究模型。     

狗冲击伤的荷载机制及效应研究

本文通过对暴露于空中爆炸波(激波)中的动物所承受不同的激波压力模态进行分析,表明处于规则反射区(NRA)与马赫反射区(MRA)中的动物的荷载机制是明显不同的。有关动物的实验结果是采用BST—Ⅰ型生物激波管致伤。其一选用44只雄性杂种狗是有端板(即NRA或MRA有反射壁)状态,另外选用8只雄性杂种狗是开口(即MRA自由场)状态。两组实验表明其创伤严重特点和创伤的分布规律都存在显著的差异。所观察到的各个器官的病理形态学和超微结构改变的动物实验结果,能够为冲击伤防护和诊治的进一步研究提供理论和临床上的依据。     

犬冲击伤早期血液流变学的变化

30只犬,用BST-Ⅰ型生物激波管致伤,以观察冲击伤早期血液流变学的变化。结果表明冲击伤早期有一过性的血液流变学改变,主要表现为血液粘度和血球压积升高、血小板粘附率增加,在伤后即刻随伤情加重而更为明显结果提示早期监测和及时处理血液流变学改变,对冲击伤的早期诊斷和救治可能有较重要的意义。     

冲击波强度与幼年大鼠肺冲击伤程度的量效关系

目的:探索冲击波强度与幼年大鼠肺冲击伤程度的量效关系,为儿童冲击伤研究提供动物模型和基础。方法:选取20天龄幼年健康SD雄鼠40只,随机分为4组:BIG1、BIG2、BIG3和BIG4,每组各10只,采用BST-Ⅰ型生物激波管以4.8~5.8 MPa驱动压致伤,观察各组动物伤后生命体征、肺大体解剖和光镜病理等,并进行肺冲击伤严重程度评分。结果:幼鼠在驱动压致伤后均出现了不同程度的呼吸急促、心率加快的表现,外耳道出血发生率为57.5%（46/80）。肺大体解剖表现为不同程度的肺出血、水肿和肺不张等。光镜下病理主要表现为不同程度的肺出血、渗出、炎症细胞的浸润、肺间质水肿增厚、肺泡内水肿和肺泡壁的断裂等。4.8 MPa驱动压时,动物所受超压峰值为433 kPa,正向冲量14 226.4 kPa[?m,肺器官损伤定级（OIS）集中在Ⅱ、Ⅲ级（40%、30%）,肺冲击伤简明损伤定级（AIS）评分为0.90±0.57,损伤程度为轻度;5.0 MPa驱动压时,超压峰值为447.7 kPa,正向冲量14 463.5 kPa[?m,OIS多集中在Ⅲ级（60%）,AIS评分为1.60±0.69,损伤程度为中度;5.5 MPa驱动压时,超压峰值为484.7 kPa,正向冲量15 017.0 kPa[?m,OIS多集中在Ⅳ级（70%）,AIS评分为3.10±0.56,损伤程度为较重;5.8 MPa驱动压时,超压峰值为506.8 kPa, 正向冲量15 325.5 kPa[?m,OIS集中在Ⅴ级（40%）附近,AIS评分为4.00±0.67,肺损伤程度为重度。各组间损伤严重程度有明显统计学差异（P<0.05）。结论:利用BST-I型生物激波管,采用4.8~5.8 MPa高压段的驱动压可建立稳定的幼年SD鼠轻~重度肺冲击伤模型。幼年大鼠肺组织对冲击波损伤的耐受性强于成年大鼠肺组织,也强于幼年兔肺组织,其机制尚不太清楚,值得进一步深入研究。     

爆炸冲击波在生物体内的传播特征

目的：了解爆炸冲击波在生物体内的传播特征。材料方法：采用压力测试方法,研究爆炸冲击波在肝、肺、血管及皮下组织内的传播特征,并与空气中的传播特征进行比较。结果：爆炸冲击波在不同介质中的衰减速度依次为：空气＞皮下组织＞血液;不同部位对爆炸冲击波感应的敏感度依次为：颅脑＞胸腔＞肝脏;颅脑内的应力感应方式不同于其他部位,以骨性震动传导为主要特征。结论：研究结果为体外模拟研究及为爆炸性冲击伤的诊断治疗提供了理论依据。     

颅脑冲击波伤血瘀证实验模型的建立

建立一种较真实模拟颅脑冲击波伤急性期血瘀证模型 ,为活血化瘀治疗颅脑冲击波伤找出理论依据。方法应用BST-1型生物激波管闭口致伤大白兔28只。伤后进行病理解剖检查 ,同时2只致伤兔局部脑血流连续监测伤前及伤后2、4、6、8、24hrCBF变化。9只兔作脑组织含水量测定。结果伤后兔脑充血肿胀以脑干为主 ,桥脑区有小出血点 ,大脑背侧有气栓。局部脑血流监测结果为2、4、6、8、24hrCBF减慢 ,伤越重 ,rCBF降低愈明显 ,脑组织含水量增高。结论本实验与1988年10月国际会议定出的血瘀证诊断标准是相似的。实验成功复制了临床颅脑冲击波伤后急性期血瘀证的特征。     

冲击伤对大鼠条件性回避反应习得和保持的影响

实验用Wistar大鼠26只,分为冲击波全身致伤组(Ⅰ组),冲击波头部致伤组(Ⅱ组)和对照组。以条件性回避反应(conditioned avoidance response,CAR)作为学习和记忆的指标,观察BST系列生物激波管产生的冲击波对CAR的影响。结果如下:(1)Ⅰ组和Ⅱ组大鼠的CAR习得率在伤后5天内均明显低于对照组(P<0.05),尤以Ⅱ组大鼠的降低更为显著(P<0.01);(2)自伤后第5天起CAR习得率便逐渐升高,至第10天时已接近对照组水平(P<0.05);(3)Ⅱ组动物CAR的保持显著低于对照组(P<0.01),而Ⅰ组仅有一过性的降低。以上结果显示,大鼠学习和记忆能力的降低主要是由于冲击波直接作用于头部的结果,但不能排除肺损伤后引起神经系统的损害。     

体内冲击波的生物力学

近来 ,生物组织细胞内的冲击波现象主要应用于结石冲击波碎石、骨成形术及各种医疗技术 ,进而正在向其它领域扩展。其中对冲击波的研究很多都集中在冲击波所具有的巨大能量及由压力而引起的变性作用且其现象在瞬间对生物体产生巨大作用 ,然而又使其不变性方面。从生物物理学及生物力学的角度看 ,其意义在于利用冲击波所具有的瞬间的压缩 -膨胀而产生的力学刺激引起生物反应。在医疗中所使用的各种冲击波 ,是由冲击波发射管产生的马赫数为 2～ 2 .5左右的冲击波 ,在管的的中间部位使管径收缩 ,以形成高压 ,并冲击放置于发射管端部的细胞。此…     

Brain Injuries from Blast

Traumatic brain injury (TBI) from blast produces a number of conundrums. This review focuses on five fundamental questions including: (1) What are the physical correlates for blast TBI in humans? (2) Why is there limited evidence of traditional pulmonary injury from blast in current military field epidemiology? (3) What are the primary blast brain injury mechanisms in humans? (4) If TBI can present with clinical symptoms similar to those of Post-Traumatic Stress Disorder (PTSD), how do we clinically differentiate blast TBI from PTSD and other psychiatric conditions? (5) How do we scale experimental animal models to human response? The preponderance of the evidence from a combination of clinical practice and experimental models suggests that blast TBI from direct blast exposure occurs on the modern battlefield. Progress has been made in establishing injury risk functions in terms of blast overpressure time histories, and there is strong experimental evidence in animal models that mild brain injuries occur at blast intensities that are similar to the pulmonary injury threshold. Enhanced thoracic protection from ballistic protective body armor likely plays a role in the occurrence of blast TBI by preventing lung injuries at blast intensities that could cause TBI. Principal areas of uncertainty include the need for a more comprehensive injury assessment for mild blast injuries in humans, an improved understanding of blast TBI pathophysiology of blast TBI in animal models and humans, the relationship between clinical manifestations of PTSD and mild TBI from blunt or blast trauma including possible synergistic effects, and scaling between animals models and human exposure to blasts in wartime and terrorist attacks. Experimental methodologies, including location of the animal model relative to the shock or blast source, should be carefully designed to provide a realistic blast experiment with conditions comparable to blasts on humans. If traditional blast scaling is appropriate between species, many reported rodent blast TBI experiments using air shock tubes have blast overpressure conditions that are similar to human long-duration nuclear blasts, not high explosive blasts.     

激波载荷下绵羊胸部动力学响应的数学模型

本文利用单自由度非线性单腔模型描述激波作用下机体胸部动力学响应,并建立其数学模型,通过测定激波作用下的绵羊胸壁内向运动的位移、速度和加速度,检验这一模型的预测效果。实验结果表明,该模型基本上反映了激波作用下绵羊胸壁运动过程,但有待于发展和完善。     

A thoracic mechanism of mild traumatic brain injury due to blast pressure waves

The mechanisms by which blast pressure waves cause mild-to-moderate traumatic brain injury (mTBI) are an open question. Possibilities include acceleration of the head, direct passage of the blast wave via the cranium, and propagation of the blast wave to the brain via a thoracic mechanism. The hypothesis that the blast pressure wave reaches the brain via a thoracic mechanism is considered in light of ballistic and blast pressure wave research. Ballistic pressure waves, caused by penetrating ballistic projectiles or ballistic impacts to body armor, can only reach the brain via an internal mechanism and have been shown to cause cerebral effects. Similar effects have been documented when a blast pressure wave has been applied to the whole body or focused on the thorax in animal models. While vagotomy reduces apnea and bradycardia due to ballistic or blast pressure waves, it does not eliminate neural damage in the brain, suggesting that the pressure wave directly affects the brain cells via a thoracic mechanism. An experiment is proposed which isolates the thoracic mechanism from cranial mechanisms of mTBI due to blast wave exposure. Results have implications for evaluating risk of mTBI due to blast exposure and for developing effective protection.     

Blast-induced neurotrauma in whales

A majority of investigations on primary blast injuries have focused on gas-containing organs, while the likelihood of blast-induced neurotrauma remains underrated. In Norway minke whales (Balaenoptera acutorostrata) are hunted using small fishing boats rigged with harpoon guns, which fire harpoons tipped with a grenade containing a charge of 30-g penthrite. The grenade detonates 60-70 cm inside the animal. The present study was undertaken to characterize the neuropathological changes caused by the penthrite blast and evaluate its role in the loss of consciousness and death in hunted whales. The study included 37 minke whales that were examined shipboard. The brains were later subjected to gross and light microscopy examination. The results showed that intra-body detonation of the grenade in near vicinity of the brain resulted in trauma similar to severe traumatic brain injury associated with a direct blow to the head. Detonation in more distant areas of the body resulted in injuries resembling acceleration-induced diffuse traumatic brain injury. The authors conclude that even if several vital organs were fatally injured in most whales, the neurotrauma induced by the blast-generated pressure waves were the primary cause for the immediate or very rapid loss of consciousness and death.     

Distribution of Blood–Brain Barrier Disruption in Primary Blast Injury

Traumatic brain injury (TBI) resulting from explosive-related blast overpressure is a topic at the forefront of neurotrauma research. Compromise of the blood–brain barrier (BBB) and other cerebral blood vessel dysfunction is commonly reported in both experimental and clinical studies on blast injury. This study used a rifle primer-driven shock tube to investigate cerebrovascular injury in rats exposed to low-impulse, pure primary blast at three levels of overpressure (145, 232, and 323 kPa) and with three survival times (acute, 24, and 48 h). BBB disruption was quantified immunohistochemically by measuring immunoglobulin G (IgG) extravasation with image analysis techniques. Pure primary blast generated small lesions scattered throughout the brain. The number and size of lesions increased with peak overpressure level, but no significant difference was seen between survival times. Despite laterally directed blast exposure, equal numbers of lesions were found in each hemisphere of the brain. These observations suggest that cerebrovascular injury due to primary blast is distinct from that associated with conventional TBI.     

Computational modeling of blast induced whole-body injury: a review

Blast injuries affect millions of lives across the globe due to its traumatic after effects on the brain and the whole body. To date, military grade armour materials are designed to mitigate ballistic and shrapnel attacks but are less effective in resisting blast impacts. In order to improve blast absorption characteristics of armours, the first key step is thoroughly understands the effects of blasts on the human body itself. In the last decade, a plethora of experimental and computational work has been carried out to investigate the mechanics and pathophysiology of Traumatic Brain Injury (TBI). However, very few attempts have been made so far to study the effect of blasts on the various other parts of the body such as the sensory organs (eyes and ears), nervous system, thorax, extremities, internal organs (such as the lungs) and the skeletal system. While an experimental evaluation of blast effects on such physiological systems is difficult, developing finite element (FE) models could allow the recreation of realistic blast scenarios on full scale human models and simulate the effects. The current article reviews the state-of-the-art in computational research in blast induced whole-body injury modelling, which would not only help in identifying the areas in which further research is required, but would also be indispensable for understanding body location specific armour design criteria for improved blast injury mitigation.     

Development of a Finite Element Model for Blast Brain Injury and the Effects of CSF Cavitation

Blast-related traumatic brain injury is the most prevalent injury for combat personnel seen in the current conflicts in Iraq and Afghanistan, yet as a research community,we still do not fully understand the detailed etiology and pathology of this injury. Finite element (FE) modeling is well suited for studying the mechanical response of the head and brain to blast loading. This paper details the development of a FE head and brain model for blast simulation by examining both the dilatational and deviatoric response of the brain as potential injury mechanisms. The levels of blast exposure simulated ranged from 50 to 1000 kPa peak incident overpressure and 1–8 ms in positive-phase duration, and were comparable to real-world blast events. The frontal portion of the brain had the highest pressures corresponding to the location of initial impact, and peak pressure attenuated by 40–60% as the wave propagated from the frontal to the occipital lobe. Predicted brain pressures were primarily dependent on the peak overpressure of the impinging blast wave, and the highest predicted brain pressures were 30%less than the reflected pressure at the surface of blast impact. Predicted shear strain was highest at the interface between the brain and the CSF. Strain magnitude was largely dependent on the impulse of the blast, and primarily caused by the radial coupling between the brain and deforming skull.The largest predicted strains were generally less than 10%,and occurred after the shock wave passed through the head.For blasts with high impulses, CSF cavitation had a large role in increasing strain levels in the cerebral cortex and periventricular tissues by decoupling the brain from the skull. Relating the results of this study with recent experimental blast testing suggest that a rate-dependent strain-based tissue injury mechanism is the source primary blast TBI.     

Chronic traumatic encephalopathy in blast-exposed military veterans and a blast neurotrauma mouse model

Blast exposure is associated with traumatic brain injury (TBI), neuropsychiatric symptoms, and long-term cognitive disability. We examined a case series of postmortem brains from U.S. military veterans exposed to blast and/or concussive injury. We found evidence of chronic traumatic encephalopathy (CTE), a tau protein-linked neurodegenerative disease, that was similar to the CTE neuropathology observed in young amateur American football players and a professional wrestler with histories of concussive injuries. We developed a blast neurotrauma mouse model that recapitulated CTE-linked neuropathology in wild-type C57BL/6 mice 2 weeks after exposure to a single blast. Blast-exposed mice demonstrated phosphorylated tauopathy, myelinated axonopathy, microvasculopathy, chronic neuroinflammation, and neurodegeneration in the absence of macroscopic tissue damage or hemorrhage. Blast exposure induced persistent hippocampal-dependent learning and memory deficits that persisted for at least 1 month and correlated with impaired axonal conduction and defective activity-dependent long-term potentiation of synaptic transmission. Intracerebral pressure recordings demonstrated that shock waves traversed the mouse brain with minimal change and without thoracic contributions. Kinematic analysis revealed blast-induced head oscillation at accelerations sufficient to cause brain injury. Head immobilization during blast exposure prevented blast-induced learning and memory deficits. The contribution of blast wind to injurious head acceleration may be a primary injury mechanism leading to blast-related TBI and CTE. These results identify common pathogenic determinants leading to CTE in blast-exposed military veterans and head-injured athletes and additionally provide mechanistic evidence linking blast exposure to persistent impairments in neurophysiological function, learning, and memory.     

Development of a Multimodal Blast Sensor for Measurement of Head Impact and Over-pressurization Exposure

It is estimated that 10–20% of United States soldiers returning from Operation Iraqi Freedom (OIF) and Operation Enduring Freedom (OEF) have suffered at least one instance of blast-induced traumatic brain injury (bTBI) with many reporting persistent symptomology and long-term effects. This variation in blast response may be related to the complexity of blast waves and the many mechanisms of injury, including over-pressurization due to the shock wave and potential for blunt impacts to the head from shrapnel or from other indirect impacts (e.g., building, ground, and vehicle). To help differentiate the effects of primary, secondary, and tertiary effects of blast, a custom sensor was developed to simultaneously measure over-pressurization and blunt impact. Moreover, a custom, complementary filter was designed to differentiate the measurements of blunt (low-frequency bandwidth) from over-pressurization (high-frequency bandwidth). The custom sensor was evaluated in the laboratory using a shock tube to simulate shock waves and a drop fixture to simulate head impacts. Both bare sensors and sensor embedded within an ACH helmet coupon were compared to laboratory reference transducers under multiple loading conditions (n = 5) and trials at each condition (n = 3). For all comparative measures, peak magnitude, peak impulse, and cross-correlation measures, R ² values, were greater than 0.900 indicating excellent agreement of peak measurements and time-series comparisons with laboratory measures.     

水下爆炸性冲击波实验模型的建立及其应力分布特性的研究

目的：建立水下爆炸性冲击波实验模型并分析其应力分布特性。方法：根据爆炸性冲击波的理论应力分布特性，建立水下爆炸性冲击波实验模型，将培养的内皮细胞放入特制的无菌薄层塑料袋内模拟细胞致伤模型，用80mg电雷管致伤后[观察细胞损伤情况。结果：爆炸性冲击波在水中的衰减速度较空气中缓慢，水的深度对冲击波压力峰值有显著影响，对于同一爆源，水越深，压力值越小，不同层数的滤膜覆盖与压力感应呈线性衰减，8层滤膜覆盖致伤时可见内皮细胞有明显的皱缩脱落现象。结论：冲击波在不同介质中的传播速度与衰减幅度与介质的密度密切相关，水下冲击波的压力值不仅与焊源的距离有关，而且与水深有关。