CAJ | 학술논문

背景:急性CO中毒大鼠可能发生迟发性健忘症,与人急性CO中毒导致的迟发性神经综合征相似,所以实验拟通过对急性CO中毒大鼠的研究来探讨迟发性神经综合征的发病机制.目的:观察急性CO中毒大鼠脑内迟发性神经元损伤和记忆功能的改变,并分析两者之间的关系.设计:随机对照动物实验.单位:解放军第四军医大学唐都医院急诊科;西安高新医院检验中心;解放军北京解放军空军总医院;解放军第四军医大学航空航天医学系高压氧治疗中心.材料:实验于2005-07/11在解放军第四军医大学航空航天医学系航空病理学和分子生物学实验室进行.取健康雄性Sprague-Dawley(SD)大鼠50只随机分为对照组和染毒组各25只.方法:将染毒组清醒大鼠放入自制染毒罐中,然后向罐内注入体积分数为0.999的CO气体.大鼠在罐内静式吸入CO与空气的混合气体,CO平均体积分数为3.451×10-3,60 min后出罐.对照组不干预.主要观察指标:①记忆能力:染毒前和暴露后1,3,5,7 d进行大鼠跳台实验,以跳台潜伏期为评价记忆保持巩固能力的指标,跳台潜伏期越短,记忆能力越差.②脑组织病理改变:暴露后1,3,5,7 d跳台实验后,两组各处死6只大鼠,取脑,行苏木精-伊红染色以观察脑内病理损伤程度和海马CA1区锥体细胞数.③应用SPSS 10.0软件分析海马CA1区锥体细胞数与组大鼠跳台潜伏期间的关系.结果:48只大鼠进入结果分析.①跳台潜伏期:CO暴露后1,3 d,两组相比没有差别,但在CO暴露后第5和7天,染毒组明显短于对照组(P＜0.05,0.01).②海马CA1区锥体细胞数:CO暴露后1 d,染毒组与正常对照相比没有明显改变,但是在CO暴露后3,5和7 d即明显减少,CO暴露后7 d,可以观察到15%的锥体细胞发生死亡.③海马CA1区锥体细胞数减少与染毒组大鼠跳台潜伏期缩短之间有明显的相关性(r=0.270,P＜0.01).具体的主要数据,研究的主要发现(给出统计学显著性检验值)结论:主要结论及其潜在的应用价值.急性CO中毒导致迟发性神经元损伤,迟发性神经元损伤引起迟发性健忘症. 揹景:急性CO中毒大鼠可能髮生遲髮性健忘癥,與人急性CO中毒導緻的遲髮性神經綜閤徵相似,所以實驗擬通過對急性CO中毒大鼠的研究來探討遲髮性神經綜閤徵的髮病機製.目的:觀察急性CO中毒大鼠腦內遲髮性神經元損傷和記憶功能的改變,併分析兩者之間的關繫.設計:隨機對照動物實驗.單位:解放軍第四軍醫大學唐都醫院急診科;西安高新醫院檢驗中心;解放軍北京解放軍空軍總醫院;解放軍第四軍醫大學航空航天醫學繫高壓氧治療中心.材料:實驗于2005-07/11在解放軍第四軍醫大學航空航天醫學繫航空病理學和分子生物學實驗室進行.取健康雄性Sprague-Dawley(SD)大鼠50隻隨機分為對照組和染毒組各25隻.方法:將染毒組清醒大鼠放入自製染毒罐中,然後嚮罐內註入體積分數為0.999的CO氣體.大鼠在罐內靜式吸入CO與空氣的混閤氣體,CO平均體積分數為3.451×10-3,60 min後齣罐.對照組不榦預.主要觀察指標:①記憶能力:染毒前和暴露後1,3,5,7 d進行大鼠跳檯實驗,以跳檯潛伏期為評價記憶保持鞏固能力的指標,跳檯潛伏期越短,記憶能力越差.②腦組織病理改變:暴露後1,3,5,7 d跳檯實驗後,兩組各處死6隻大鼠,取腦,行囌木精-伊紅染色以觀察腦內病理損傷程度和海馬CA1區錐體細胞數.③應用SPSS 10.0軟件分析海馬CA1區錐體細胞數與組大鼠跳檯潛伏期間的關繫.結果:48隻大鼠進入結果分析.①跳檯潛伏期:CO暴露後1,3 d,兩組相比沒有差彆,但在CO暴露後第5和7天,染毒組明顯短于對照組(P＜0.05,0.01).②海馬CA1區錐體細胞數:CO暴露後1 d,染毒組與正常對照相比沒有明顯改變,但是在CO暴露後3,5和7 d即明顯減少,CO暴露後7 d,可以觀察到15%的錐體細胞髮生死亡.③海馬CA1區錐體細胞數減少與染毒組大鼠跳檯潛伏期縮短之間有明顯的相關性(r=0.270,P＜0.01).具體的主要數據,研究的主要髮現(給齣統計學顯著性檢驗值)結論:主要結論及其潛在的應用價值.急性CO中毒導緻遲髮性神經元損傷,遲髮性神經元損傷引起遲髮性健忘癥.
배경:급성CO중독대서가능발생지발성건망증,여인급성CO중독도치적지발성신경종합정상사,소이실험의통과대급성CO중독대서적연구래탐토지발성신경종합정적발병궤제.목적:관찰급성CO중독대서뇌내지발성신경원손상화기억공능적개변,병분석량자지간적관계.설계:수궤대조동물실험.단위:해방군제사군의대학당도의원급진과;서안고신의원검험중심;해방군북경해방군공군총의원;해방군제사군의대학항공항천의학계고압양치료중심.재료:실험우2005-07/11재해방군제사군의대학항공항천의학계항공병이학화분자생물학실험실진행.취건강웅성Sprague-Dawley(SD)대서50지수궤분위대조조화염독조각25지.방법:장염독조청성대서방입자제염독관중,연후향관내주입체적분수위0.999적CO기체.대서재관내정식흡입CO여공기적혼합기체,CO평균체적분수위3.451×10-3,60 min후출관.대조조불간예.주요관찰지표:①기억능력:염독전화폭로후1,3,5,7 d진행대서도태실험,이도태잠복기위평개기억보지공고능력적지표,도태잠복기월단,기억능력월차.②뇌조직병리개변:폭로후1,3,5,7 d도태실험후,량조각처사6지대서,취뇌,행소목정-이홍염색이관찰뇌내병리손상정도화해마CA1구추체세포수.③응용SPSS 10.0연건분석해마CA1구추체세포수여조대서도태잠복기간적관계.결과:48지대서진입결과분석.①도태잠복기:CO폭로후1,3 d,량조상비몰유차별,단재CO폭로후제5화7천,염독조명현단우대조조(P＜0.05,0.01).②해마CA1구추체세포수:CO폭로후1 d,염독조여정상대조상비몰유명현개변,단시재CO폭로후3,5화7 d즉명현감소,CO폭로후7 d,가이관찰도15%적추체세포발생사망.③해마CA1구추체세포수감소여염독조대서도태잠복기축단지간유명현적상관성(r=0.270,P＜0.01).구체적주요수거,연구적주요발현(급출통계학현저성검험치)결론:주요결론급기잠재적응용개치.급성CO중독도치지발성신경원손상,지발성신경원손상인기지발성건망증.
BACKGROUND:Acute carbon monoxide (CO) poisoning may lead to delayed amnesia in rats,and which is similar to delayed neurologic syndrome caused by acute CO in human.So,this experiment is to investigate the pathogenesis of delayed neurologic syndrome by studying acute CO poisoning in the rats.OBJECTIVE:To observe the changes in delayed neuronal damage and memory after acute CO poisoning in the rats,and analyze their correlation.DESIGN:Randomized controlled animal experiment.SETTING:Department of Emergency,Tangdu Hospital,Fourth Military Medical University of Chinese PLA;Department of Laboratory Medicine,Xi'an Gaoxin Hospital;The General Hospital of the Air Force of Chinese PLA,Center for Hyperbaric Oxygen Treatment,Department of Aerospace Medicine,Fourth Military Medical University of Chinese PLA.MATERIALS:This experiment was carried out in the Laboratory of Aviation Pathology and Molecular Biology,Department of Aerospace Medicine.Fourth Military Medical University of Chinese PLA from July to November 2005.Fiftyhealthy male Sprague-Dawley(SD)rats were randomized into control group and CO poisoning group,with 25 rats each.METHODS:The awake rats in the CO poisoning group were placed in self-made jar for poisoning,then which was pumped with 0.999 volume fraction of CO.Rats in the jar inhaled the mixture of CO and air for 60 minutes.The average volume fraction of CO in the jar was 3.451×10-3.Rats in the control group were untouched.MAIN OUTCOME MEASURES:①The step down test was carried out in the rats before and 1,3,5 and 7 days after Coexposure.Escape latency was used as an index for evaluating the ability of memory retention.Shorter escape latencyindicated poor memory ability.②Pathological changes of brain tissue:After step down test was carried out following 1,3,5 and 7 days of CO exposure,6 rats were separately sacrificed in each group,and their brains were harvested.The brain tissue sections were performed haematoxylin & eosin (HE) staining for observing pathological injury degree and the amount of pyramidal neurons in hippocampal CA1 region.③SPSS 10.0 software was used to analyze the relationship of the amount of pyramidal neurons in hippocampal CA1 region and escape latency.RESULTS:Forty-eight rats were involved in the final analysis.①There were no significant differences in escape latencyon the 1"and 3"days after CO exposure between two groups. but escape latency in the CO poisoning group was significantly shorter than that in the control group on the 5th and 7th days after CO exposure(P＜0.05,0.01).②There were no significant changes in the amount of pyramidal neurons in hippocampal CA1 region on the 1st day after CO exposure between CO poisoning group and control group,but pyramidal neurons in hippocampal CA1 region in the CO poisoning group were significantly reduced on the 3rd,5th and 7th days after CO exposure,and 1 5%dead pyramidal neurons were found on the 7th day after CO exposure.③Decrease of pyramidal neurons in hippocampal CA1 region was significantly correlated with shortening of escape latency of rats in the CO poisoning group(r=0.270,P＜0.01).CONCLUSION:Acute CO poisoning leads to delayed neuronal damage,which causes delayed amnesia.