A new model to produce sagittal plane rotational induced diffuse axonal injuries.
A new model to produce sagittal plane rotational induced diffuse axonal injuries.
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DOI：
10.3389/fneur.2011.00041
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发表时间：
2011
影响因子：
3.4
通讯作者：
Risling M
中科院分区：
文献类型：
--
作者：
Davidsson J;Risling M
建立了一种新的矢状面后向旋转加速度造成弥漫性脑损伤的体内动物模型。在这个模型中，一只被麻醉的成年大鼠的头骨被紧紧地固定在一个旋转的棒上。在创伤中，棒子受到撞击，导致棒子和动物头部向后旋转；加速阶段持续0.4毫秒，随后以恒定速度旋转，当杆与填充停止接触时，缓慢减速。总水头角度变化小于30°。通过调整步枪内用于加速前锋的气压，可以产生0.3和2.1 Mrad/s2之间的旋转加速度。创伤水平、创伤后生存时间、脑和血清检索以及组织制备技术的多种组合被用来表征这个新模型。这种创伤导致暴露于严重创伤的动物出现硬膜下出血。用β-淀粉样前体蛋白抗体和FD神经银对脑组织进行染色，发现在胼胝体、胼胝体与皮层交界处以及脑干束中广泛存在轴突损伤（AI）。仅当旋转加速度水平为中等及以上时，观察到的AIs才明显。相反，创伤后仅观察到有限的挫伤迹象。巨噬细胞侵袭、胶质原纤维酸性蛋白重分布或肥大、血脑屏障（BBB）改变不常见。S100血清分析表明，尽管没有明显的血脑屏障损伤，但中度创伤后仍会发生血管和胶质细胞损伤。我们的结论是，这种旋转创伤模型能够产生分级轴索损伤，可重复，并产生有限的其他类型的创伤性脑损伤，因此在弥漫性轴索损伤后的损伤生物力学、诊断和治疗策略的研究中是有用的。
A new in vivo animal model that produces diffuse brain injuries in sagittal plane rearward rotational acceleration has been developed. In this model, the skull of an anesthetized adult rat is tightly secured to a rotating bar. During trauma, the bar is impacted by a striker that causes the bar and the animal head to rotate rearward; the acceleration phase last 0.4 ms and is followed by a rotation at constant speed and a gentle deceleration when the bar makes contact with a padded stop. The total head angle change is less than 30°. By adjusting the air pressure in the rifle used to accelerate the striker, resulting rotational acceleration between 0.3 and 2.1 Mrad/s2 can be produced. Numerous combinations of trauma levels, post-trauma survival times, brain and serum retrieval, and tissue preparation techniques were adopted to characterize this new model. The trauma caused subdural bleedings in animals exposed to severe trauma. Staining brain tissue with β-Amyloid Precursor Protein antibodies and FD Neurosilver that detect degenerating axons revealed wide spread axonal injuries (AI) in the corpus callosum, the border between the corpus callosum and cortex and in tracts in the brain stem. The observed AIs were apparent only when the rotational acceleration level was moderate and above. On the contrary, only limited signs of contusion injuries were observed following trauma. Macrophage invasions, glial fibrillary acidic protein redistribution or hypertrophy, and blood brain barrier (BBB) changes were unusual. S100 serum analyses indicate that blood vessel and glia cell injuries occur following moderate levels of trauma despite the absence of obvious BBB injuries. We conclude that this rotational trauma model is capable of producing graded axonal injury, is repeatable and produces limited other types of traumatic brain injuries and as such is useful in the study of injury biomechanics, diagnostics, and treatment strategies following diffuse axonal injury.