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首页> 美国卫生研究院文献>Frontiers in Neurology >Neuro-Glial and Systemic Mechanisms of Pathological Responses in Rat Models of Primary Blast Overpressure Compared to Composite Blast
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Neuro-Glial and Systemic Mechanisms of Pathological Responses in Rat Models of Primary Blast Overpressure Compared to Composite Blast

机译：与复合冲击波相比原发冲击波超压大鼠模型中神经胶质和病理反应的全身机制

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A number of experimental models of blast brain injury have been implemented in rodents and larger animals. However, the variety of blast sources and the complexity of blast wave biophysics have made data on injury mechanisms and biomarkers difficult to analyze and compare. Recently, we showed the importance of rat position toward blast generated by an external shock tube. In this study, we further characterized blast producing moderate traumatic brain injury and defined “composite” blast and primary blast exposure set-ups. Schlieren optics visualized interaction between the head and a shock wave generated by external shock tube, revealing strong head acceleration upon positioning the rat on-axis with the shock tube (composite blast), but negligible skull movement upon peak overpressure exposure off-axis (primary blast). Brain injury signatures of a primary blast hitting the frontal head were assessed and compared to damage produced by composite blast. Low to negligible levels of neurodegeneration were found following primary blast compared to composite blast by silver staining. However, persistent gliosis in hippocampus and accumulation of GFAP/CNPase in circulation was detected after both primary and composite blast. Also, markers of vascular/endothelial inflammation integrin alpha/beta, soluble intercellular adhesion molecule-1, and L-selectin along with neurotrophic factor nerve growth factor-beta were increased in serum within 6 h post-blasts and persisted for 7 days thereafter. In contrast, systemic IL-1, IL-10, fractalkine, neuroendocrine peptide Orexin A, and VEGF receptor Neuropilin-2 (NRP-2) were raised predominantly after primary blast exposure. In conclusion, biomarkers of major pathological pathways were elevated at all blast set-ups. The most significant and persistent changes in neuro-glial markers were found after composite blast, while primary blast instigated prominent systemic cytokine/chemokine, Orexin A, and Neuropilin-2 release, particularly when primary blast impacted rats with unprotected body.
机译：已经在啮齿动物和较大的动物中实施了许多爆炸性脑损伤的实验模型。然而，爆炸源的多样性和爆炸波生物物理学的复杂性使得关于伤害机制和生物标志物的数据难以进行分析和比较。最近，我们展示了老鼠位置对于外部震动管产生爆炸的重要性。在这项研究中，我们进一步表征了爆炸产生中度创伤性脑损伤的情况，并定义了“复合”爆炸和原始爆炸暴露设置。 Schlieren光学器件可视化了头部和外部电击管产生的电击波之间的相互作用，揭示了在将大鼠与电击管同轴放置时的强劲头部加速度（复合爆炸），但在峰值超压暴露离轴时颅骨运动可忽略不计（主要）爆破）。评估了撞击头部的原始爆炸的脑损伤特征，并将其与复合爆炸产生的损伤进行了比较。与通过银染的复合爆炸相比，原发爆炸后发现的神经变性水平低至可忽略不计。然而，在原发性和复合性爆炸后均检测到海马持续胶质细胞增生和循环中GFAP / CNPase的积累。同样，在爆炸后6小时之内，血清中血管/内皮炎症整合素α/β，可溶性细胞间粘附分子-1和L-选择素以及神经营养因子神经生长因子-β的标记物在血清中增加，并在此后持续7天。相比之下，全身性IL-1，IL-10，fractalkine，神经内分泌肽Orexin A和VEGF受体Neuropilin-2（NRP-2）主要在初次爆炸暴露后升高。总之，在所有冲击波设置下，主要病理途径的生物标志物均升高。在复合冲击波后，神经胶质标记物发生了最显着，最持久的变化，而原始冲击波则促使系统性细胞因子/趋化因子，Orexin A和Neuropilin-2的释放显着，尤其是当原始冲击波冲击了未保护身体的大鼠时。

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