小型动物重症胸部创伤模型撞击装置

A mechanical device for animal impact injury experiment and establish a rodent model of severe thoracic injury

目的设计制作小型动物撞击装置，并以此为基础建立了大鼠重症胸部创伤模型。方法自行设计制作小型生物撞击装置，测量撞击速度的误差以及撞击中心点的圆周误差。将成年雄性SD大鼠84只，随机平均分配到A、B、C、D、E、F、G共7组，用自行设计制作的小型生物撞击装置撞击致伤。A组为对照组，进行假撞击；其余各组以不同的撞击速度和胸廓压缩比为撞击条件：B组（3m／s，20％），C组（3m／s，40％），D组（6m／s，20％），E组（6m／s，40％），F组（9m／s，20％），G组（9m／s，40％）；定位于右腋前线第3、4肋间进行水平状态准静态撞击。大鼠撞击前、撞击后2h、撞击后12h，分别进行动脉血气分析。撞击后12h处死所有大鼠，开胸判断伤情并评分后取出肺脏，右肺损伤区域取材行病理学检查。结果该撞击装置的撞击速度误差〈4％，撞击中心点圆周误差〈3mm。大鼠撞击后一般表现为：血压、心率即刻下降，然后迅速恢复或超过伤前水平；呼吸暂停，之后出现浅快呼吸。动脉血气分析提示：撞击后B、C组大鼠出现低碳酸血症；D、E、F组大鼠出现低碳酸血症合并低氧血症，其中E组大鼠变化最为明显且持续时间较长。大鼠胸部伤情判断评分发现：A组（0分），无胸部损伤；B组（1．50±0．52）分、C组（1．92±0．67）分、D组（2．58±0．67）分，创伤均轻微，12h内无死亡；E组（4．08±0．90）分，创伤较重，12h死亡率为33．33％；F组（3．08±0．79）分，创伤较轻，12h死亡率为8．33％；G组（5．25±0．62）分，创伤极重，12h死亡率为83．33％。病理检查见损伤区域肺组织结构破坏明显，肺泡内广泛出血，肺泡间质水肿，炎症细胞的浸润。结论该动物撞击装置撞击参数控制准确，重复性好。以撞击速度6m／s、胸廓压缩比40％为撞击条件，建立的大鼠胸部创伤模型可以模拟临床所见的重症胸部创伤患者的典型病理生理过程，稳定可靠，适用于撞击所致的胸部重症创伤及其继发性损伤反应的相关研究。

Objective Direct impact is a common mechanism of injury for blunt thoracic injury, and if resuhing thoracic injury is severe the mortality may be as high as 10% -25% .We aim to develop a mechanical device for animal impact injury experiment, so as to establish a rodent model of severe thoracic injury. Method A spring operated mechanical device for animal impact injury experiment was developed. The device allowed for accurate controlled delivery of impact force to specific areas of the chest well, at specific velocities and degrees of chest compression. Eighty-four male Sprague-Dawley rats were anaesthetized and underwent left carotid artery cannulation. They were randomly divided into seven groups and given the following treatment： group A （Control group） were subjected to sham impact;group B to G animals were subjected to impacts on the right lateral superior chest at different velocities and degrees of chest wall compression. （B 3 m/s, 20% ; C 3 m/s 40% ; D 6 m/s 20% ; E 6 m/s 40% ; F 9 m/s 20% ; G 9 m/s d0% ）. Arterial blood gas samples were taken just before injury, and at 2 and 12 post injury. All rats were sacrificed at 12 hours and their degree of thoracic injury rated. Pathological examination of injured lung tissue was also performed. Results The device was able to deliver impact forces accurately, with 〈 4% deviation from desired velocity and 〈 3 mm deviation from target area of impact. Other than the control group, all animals experienced significant hemedynamic changes immediately post impact. Arterial blood gas analysis detected significant hypocapnia in groups B and C. Significant hypoxemia and hypocapnia was detected in groups D, E and F. In groups B, C, D and F, the impact produced a mild thoracic injury with low mortality rate at 12 hours. In group E, the impact produced severe thoracic injury with mortality rate of 33.33% at 12 hours. Group G animals sustained the most serious thoracic injury with mortality rate of 83.33% at 12 hours. Pathological examination revealed injuries from direct trauma as well as secondary lung injuries. Conclusions Our device was able to repetitively deliver accurate and precise impact forces to rats and allows us to establish a rodent model of severe thoracic injury from blunt trauma. We found that with our device,impact force at velocity of 6 m/s and 40% chest compression produced the most severe lung injury in rats.This helps us establish a rodent model of severe thoracic injury which can be use for future research in severe blunt thoracic trauina and the secondary lung injuries.