中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2008年
9期
935-939
,共5页
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(3 m/s,20%),C组(3 m/s,40%),D组(6 m/s,20%),E组(6 m/s,40%),F组(9 m/s,20%),G组(9 m/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2 h、撞击后12 h,分别进行动脉血气分析.撞击后12 h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,12 h内无死亡;E组(4.08±0.90)分,创伤较重,12 h死亡率为33.33%;F组(3.08±0.79)分,创伤较轻,12 h死亡率为8.33%;G组(5.25±0.62)分,创伤极重,12 h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6 m/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.
目的 設計製作小型動物撞擊裝置,併以此為基礎建立瞭大鼠重癥胸部創傷模型.方法 自行設計製作小型生物撞擊裝置,測量撞擊速度的誤差以及撞擊中心點的圓週誤差.將成年雄性SD大鼠84隻,隨機平均分配到A、B、C、D、E、F、G共7組,用自行設計製作的小型生物撞擊裝置撞擊緻傷.A組為對照組,進行假撞擊;其餘各組以不同的撞擊速度和胸廓壓縮比為撞擊條件:B組(3 m/s,20%),C組(3 m/s,40%),D組(6 m/s,20%),E組(6 m/s,40%),F組(9 m/s,20%),G組(9 m/s,40%);定位于右腋前線第3、4肋間進行水平狀態準靜態撞擊.大鼠撞擊前、撞擊後2 h、撞擊後12 h,分彆進行動脈血氣分析.撞擊後12 h處死所有大鼠,開胸判斷傷情併評分後取齣肺髒,右肺損傷區域取材行病理學檢查.結果 該撞擊裝置的撞擊速度誤差＜4%,撞擊中心點圓週誤差＜3mm.大鼠撞擊後一般錶現為:血壓、心率即刻下降,然後迅速恢複或超過傷前水平;呼吸暫停,之後齣現淺快呼吸.動脈血氣分析提示:撞擊後B、C組大鼠齣現低碳痠血癥;D、E、F組大鼠齣現低碳痠血癥閤併低氧血癥,其中E組大鼠變化最為明顯且持續時間較長.大鼠胸部傷情判斷評分髮現:A組(0分),無胸部損傷;B組(1.50±0.52)分、C組(1.92±0.67)分、D組(2.58±0.67)分,創傷均輕微,12 h內無死亡;E組(4.08±0.90)分,創傷較重,12 h死亡率為33.33%;F組(3.08±0.79)分,創傷較輕,12 h死亡率為8.33%;G組(5.25±0.62)分,創傷極重,12 h死亡率為83.33%.病理檢查見損傷區域肺組織結構破壞明顯,肺泡內廣汎齣血,肺泡間質水腫,炎癥細胞的浸潤.結論 該動物撞擊裝置撞擊參數控製準確,重複性好.以撞擊速度6 m/s、胸廓壓縮比40%為撞擊條件,建立的大鼠胸部創傷模型可以模擬臨床所見的重癥胸部創傷患者的典型病理生理過程,穩定可靠,適用于撞擊所緻的胸部重癥創傷及其繼髮性損傷反應的相關研究.
목적 설계제작소형동물당격장치,병이차위기출건립료대서중증흉부창상모형.방법 자행설계제작소형생물당격장치,측량당격속도적오차이급당격중심점적원주오차.장성년웅성SD대서84지,수궤평균분배도A、B、C、D、E、F、G공7조,용자행설계제작적소형생물당격장치당격치상.A조위대조조,진행가당격;기여각조이불동적당격속도화흉곽압축비위당격조건:B조(3 m/s,20%),C조(3 m/s,40%),D조(6 m/s,20%),E조(6 m/s,40%),F조(9 m/s,20%),G조(9 m/s,40%);정위우우액전선제3、4륵간진행수평상태준정태당격.대서당격전、당격후2 h、당격후12 h,분별진행동맥혈기분석.당격후12 h처사소유대서,개흉판단상정병평분후취출폐장,우폐손상구역취재행병이학검사.결과 해당격장치적당격속도오차＜4%,당격중심점원주오차＜3mm.대서당격후일반표현위:혈압、심솔즉각하강,연후신속회복혹초과상전수평;호흡잠정,지후출현천쾌호흡.동맥혈기분석제시:당격후B、C조대서출현저탄산혈증;D、E、F조대서출현저탄산혈증합병저양혈증,기중E조대서변화최위명현차지속시간교장.대서흉부상정판단평분발현:A조(0분),무흉부손상;B조(1.50±0.52)분、C조(1.92±0.67)분、D조(2.58±0.67)분,창상균경미,12 h내무사망;E조(4.08±0.90)분,창상교중,12 h사망솔위33.33%;F조(3.08±0.79)분,창상교경,12 h사망솔위8.33%;G조(5.25±0.62)분,창상겁중,12 h사망솔위83.33%.병리검사견손상구역폐조직결구파배명현,폐포내엄범출혈,폐포간질수종,염증세포적침윤.결론 해동물당격장치당격삼수공제준학,중복성호.이당격속도6 m/s、흉곽압축비40%위당격조건,건립적대서흉부창상모형가이모의림상소견적중증흉부창상환자적전형병리생리과정,은정가고,괄용우당격소치적흉부중증창상급기계발성손상반응적상관연구.
Objective Direct impact is a common mechanism of injury for blunt thoracic injury, and if resulting 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. Eghty-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 40%). 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 hemodynamic 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, die 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 C 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 firm 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 trauma and the secondary lung injuries.
