固定双上肢并悬挂家兔死亡机理的研究

目的观测固定双上肢并悬挂家兔的血气变化及膈肌的肌电变化,探讨体位性窒息死亡的发生机制。方法建立家兔体位性窒息死模型,在实验前、后分别抽取家兔耳缘动脉和左心室血2m l进行血气分析,并监测实验过程中家兔膈肌肌电图(EMGd i)的变化。结果实验组与对照组均有缺氧、二氧化碳储留以及氧饱和度下降,但是实验组的二氧化碳储留比对照组低,氧饱和度比对照组高,缺氧情况比对照组低。在连续记录的EMGd i中,早期EMGd i较晚期EMGd i的高频与低频(H/L)比值显著降低,超过20%。结论固定双上肢并悬挂家兔死亡与膈肌疲劳导致缺氧窒息有关     

悬挂双前肢致死兔的膈肌超微结构的研究

目的研究悬挂体位下窒息死亡动物的膈肌超微结构变化。方法取悬挂双前肢体位家兔的膈肌和腓肠肌组织,以勒颈致死家兔的膈肌和腓肠肌组织为对照,采用透射电镜方法观察其超微结构的变化。结果悬挂组膈肌的细胞核、细胞质、细胞膜均有缺氧损伤的征象,其中肌纤维内的肌原纤维、线粒体病变尤为严重;勒颈组膈肌的改变与悬挂组膈肌相类似,但程度上较轻微;悬挂组腓肠肌轻微病变,但肌原纤维无明显改变;勒颈组腓肠肌无明显改变。结论悬挂体位造成了膈肌纤维超微结构的损伤,形成了机体缺氧的病理基础,可导致死亡;本实验的结果可为限制性体位窒息死亡的法医学鉴定标准提供实验性的形态学依据。     

家兔限制性体位窒息模型中的LDH/CHE活性变化

目的 探讨家兔体位性窒息模型中乳酸脱氢酶(LDH)和胆碱脂酶(CHE)活性变化与窒息死亡的关系。方法 建立动物模型，检测膈肌、腓肠肌，以及血清中LDH、CHE的活性变化。结果 实验组家兔膈肌与腓肠肌相比，LDH活性明显下降，且差异显著(P＜0.05)，CHE活性差异无显著性(P＞0.05)；2组膈肌比较，LDH活性明显下降，有显著性差异(P＜0.05)，CHE活性无显著性差异(P＞0.05)；实验组血清中LDH活性比对照组明显升高，有显著性差异(P＜0.05)，2组CHE活性无显著性差异(P＞0.05)。结论 膈肌中LDH活性的降低与固定双上肢悬挂体位具有相关性。     

兔悬挂双前肢致死组织中PKC、AchE、HSP70的活性变化

目的观察兔悬挂双前肢致死不同组织中PKC、AchE、HSP70的活性变化,探讨其在死亡机制中的作用。方法家兔双前肢悬挂致死亡,取膈肌、肋间肌、心肌、腓肠肌、大脑、脑干、肝、肾、肺等组织,以勒颈、颅脑损伤和疾病死亡相应组织为对照。采用SP法对上述组织中蛋白激酶C(PKC)、乙酰胆碱酯酶(AchE)和热休克蛋白70(HSP70)进行免疫组化染色,观察其活性,并采用多组独立样本的Kruskal-Wallis秩和检验方法,对结果进行统计学分析。结果膈肌、肋间肌和大脑组织细胞质中PKC免疫组化阳性染色,悬挂组较其它组增强(P0.05);膈肌、肋间肌、心肌、大脑和肝细胞质及肌组织神经束中AchE免疫组化阳性染色,悬挂组较其它组增强(P0.05);大脑、心、肺中HSP70免疫组化阳性染色,悬挂组较其它组增强(P0.05)。结论PKC、AChE、HSP70通过不同机制,在悬挂双上肢体位性窒息死亡中起到一定作用,本文结果可为相关研究及鉴定提供实验依据。     

膈肌疲劳在家兔体位窒息死亡中的作用

目的探讨膈肌在固定双上肢悬挂致死中的作用。方法将家兔固定双上肢悬挂,并监测家兔膈肌肌电图(EMGdi)的变化。结果在连续记录的EMGdi中早期的EMGdi与晚期的EMGdi比较高频与低频(H/L)的比值显著降低,提示膈肌疲劳确实存在。结论膈肌疲劳在固定双上肢悬挂致死中起着重要的作用。     

限制性体位窒息死亡的法医学鉴定

限制性体位窒息是一种特殊类型的窒息,其死亡机理、过程复杂,体表损伤轻微,尸体表现缺乏特异性,鉴定难度大,目前还没有一个客观、准确、公认的鉴定标准,通过文献复习总结有关体位性窒息的研究成果,结合窒息死亡的组织病理改变和鉴定实践,提出限制性体位窒息的检验鉴定要点,在确定有长时间限定在某一影响呼吸的体位,且自己不能解脱;有明显的窒息尸体征象;排除损伤、疾病致死;常见毒物检测阴性;膈肌Fn免疫荧光检测阳性或透射电镜检查证明有膈肌损伤的可以诊断。如果合并有损伤或疾病,还应该有肺SP-A检查阳性或HIF1-α免疫组化染色核阳性表达。某些特定部位的损伤检查有助于分析体位关系。     

体位性窒息对心、肺功能影响的实验研究

通过从股静脉将漂浮导管插入肺动脉的方法 ,检测悬挂前、悬挂期间和临终阶段呼吸、肺动脉压、心输出量的变化,探讨体位性窒息对心、肺功能影响及其在死亡中所起作用。结果:(1)悬挂前呼吸频率平稳 ,悬挂期间逐渐加快 ,临终前呈无规律状态 ;(2)悬挂期间及临终时肺动脉压比悬挂前明显升高;(3)悬挂前及悬挂期间的心输出量基本平稳 ,临终时比悬挂前及悬挂期间明显下降。本研究发现 ,悬挂可致呼吸失调 ,机体缺氧 ,导致心、肺功能障碍 ,属肺性死亡。其特征为呼吸停止是原发性的 ,心跳停止是继发的。     

固定双上肢悬挂致死机理初探

为探索固定双上肢悬挂致死的死因及其死亡机理，本研究对１０只家兔进行案例的模拟实验及血气分析．实验结果表明：实验动物悬挂一段时间后开始出现紫绀、呼吸困难、呼吸停止，继而心跳停止、实验后与实验前相比，ＰＨ值、ＰａＯ２、ＨＣＯ３－、ＢＥ水平明显下降（Ｐ＜０．０５，Ｐ＜０．０１）；ＰａＣＯ２、Ｋ＋、Ｃａ２＋水平明显升高（Ｐ＜０．０１）．这说明其死因属窒息死．其死亡机理为固定双上肢悬挂后，呼吸肌协调失常致呼吸衰竭死亡．     

重伤家兔体内Cu及代谢酶变化与MOF及死亡关系

目的探讨兔重伤后机体内铜（Cu）含量及其代谢酶铜锌超氧化物歧化酶（Cu/Zn-SOD）、细胞色素c氧化酶（CCO）活性变化与继发性多器官衰竭（MOF）及死亡的关系。方法参照国际通用的创伤程度量化评分标准（ISS）,建立致MOF的家兔重伤模型,检测伤后不同时段血清及组织Cu含量与Cu/Zn-SOD和CCO的活性,分析其变化规律与继发MOF及死亡的关系。结果①重伤组家兔（包括死亡组家兔）血清Cu含量在伤后12h显著下降,36h后逐步回复;脑、心、肺组织中Cu含量伤后下降,肝脏组织Cu含量于伤后12h显著升高,36h后回落。伤后死亡组家兔脑、心、肺、肝Cu含量均较对照组降低,其中脑、肝组织Cu含量下降显著。②重伤组家兔血清Cu/Zn-SOD活性伤后12h下降3,6h之后呈升高的趋势,肝脏组织中的Cu/Zn-SOD活性伤后持续显著升高。③重伤后家兔（包括死亡组家兔）大脑皮质、心、肝CCO活性变化不明显,但脑干组织CCO活性显著升高。伤后死亡组家兔脑、心、肺、肝等器官的大体及组织学呈MOF改变。结论严重创伤可引发兔血清和组织Cu水平及Cu/Zn-SOD、CCO活性变化,这些变化可能与继发多器官衰竭和死亡相关。     

挤压家兔后肢导致急性肝损伤和抗氧化能力降低

目的本实验观察挤压家兔后肢导致肝氧化损伤,探讨氧化应激在挤压家兔后肢导致肝损伤中的作用。方法用标准重物间断压迫家兔后肢复制模型。采用生化方法检测ALT和AST活性;分析天平称重方法检测肝脏湿干重比值(W/D);比色法测定肝组织超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)活性和总抗氧化能力(T-AOC)以及丙二醛(MDA)含量变化;并观察肝组织病理学改变。结果血清ALT和AST活性明显增高(P<0.01),肝细胞明显肿胀,肝窦轻度淤血,而肝脏湿干重比值(W/D)轻度增加(P<0.05);肝脏氧化损伤明显加重,MDA含量增高,而肝脏抗氧化能力下降,SOD、CAT、GSH-Px活性和T-AOC分别比对照组降低了17%、29%、24%和21%(P均<0.01)。结论挤压家兔后肢引起急性肝损伤及肝脏的抗氧化能力下降;肝脏局部抗氧化能力下降可能是肝损伤的重要因素。     

An experimental study of death in a reverse suspension.

To investigate the course of respiration and circulation in a head-down position, 14 rabbits were set in reverse suspension. The respiratory rate increased a little, but the amplitude of the respiratory movements did not change in the beginning of the experiment. The amplitude of respiratory movements then began to reduce gradually, and toward the end of the experiment, it reduced suddenly. PaO2 increased in the beginning of the experiment and then began to decrease in accordance with the reduction of the amplitude of the respiratory movements. The blood pressure decreased with relation to the decrease of PaO2 resulting from the reduction of the amplitude of the respiratory movements. All rabbits died in 17 to 44 hours (average, 26 hours). The results suggested that the cause of death in a head-down position is due to postural asphyxia resulting from hindered respiratory movements, and that it is possible to survive for at least half a day in a head-down position.     

周围神经损伤MCV测定及其法医学意义

目的探讨周围神经损伤后运动神经传导速度(MCV)改变与靶肌肌力级别的相关性。方法 60例病程6个月以上的单侧肢体神经损伤(正中神经12例、尺神经13例、桡神经13例、腓浅神经12例、腓深神经10例)患者,根据Lovett肌力0～5级分级标准,确定受损神经支配的靶肌的肌力;采用DNI-200+型肌电诱发仪行患侧与健侧肢体MCV检查,观察不同级别肌力靶肌MCV指标变化。结果所测5种神经MCV各指标(健侧-患侧)/健侧变化率均与靶肌肌力呈逐渐降低的变化趋势,存在显著负相关性,其中波幅和面积下降率在肌力2级与3级、4级与5级组间存在显著性差异(P<0.05)。潜伏期延长率和传导速度下降率在肌力1级与2级、4级与5级组间存在显著性差异(P<0.05)。结论 MCV与周围神经损伤有较好的相关性,可用于推断神经受损程度,并有助于肌力级别的判定,是评价周围神经损伤程度的客观方法。     

图形异同判别ERP技术检测伪装认知损害的研究

目的探讨图形异同判别ERP范式对鉴别伪装认知损害的法医学价值。方法 40例健康志愿者在合作和伪装认知损害两种情境下,进行二项必选数字记忆测验(BFDMT)及图形异同判别ERP范式检测,对照组为20例合作的三级脑外伤者。结果三组被试完成相同、无关、相似图形刺激后引出的ERP波均包括N1、P2、N2、P3和N3五个成分,三组样本组间的N2、P3和N3的潜伏期和波幅均存在差异。其中,伪装组相同图形的N3潜伏期与正常组无显著性差异,明显短于外伤组(P<0.01);伪装组无关图形的N3潜伏期较正常组延长,但短于外伤组,波幅较正常组降低(P<0.05);伪装组相似图形的N3潜伏期较正常组和外伤组缩短(P<0.01),波幅较正常组降低(P<0.01)。以N3潜伏期为指标进行判别分析,探查伪装认知损害的敏感性为81.8%、特异性为76.9%、命中率为79.2%。结论图形异同判别范式可引出稳定的特征性ERP成分,其中N3的波幅和潜伏期有显著的组间差异,对判断伪装认知损害有一定的参考价值。     

Study on the changes of electrocardiogram and ultrastructural in heroin dependence in rats

OBJECTIVE: To study the changes of electrocardiograms (ECG) and myocardial ultrastructure in heroin dependence in rats, in order to reveal the mechanisms of the myocardial injury by heroin. METHODS: Establish heroin addict model in SD mice, investigate the changes in electrocardiograms, HE staining and myocardial ultrastructure. RESULTS: The electrocardiograms of the addict group had prominently changes, main expressions: heart rate decreased, P wave and T wave amplitude reduced and duration increased, S-T reduced and duration increased, QT interval prolongation, these changes indicated that myocardium had been injured, myocardial ischemia, ventricle function declined. These difference was significant (P<0.05) between before inject heroin and after inject heroin. Transformations in the ultrastructure: nuclear concentrate, reduce, nuclear membrane shrink, chromatin agglutinate, mitochondria cristal had disorder formation, disappeared or hollowed, these indicated that heroin could cause pathological changes in myocardial ultrastructure. CONCLUSION: Above-mentioned changes indicated that heroin can injure myocardium, and the changes of myocardial ultrastructure suggested that myocardial apoptosis may be one of the mechanisms of the myocardial injury by heroin.     

阴茎体感诱发电位在法医鉴定中的应用价值

目的探讨阴茎体感诱发电位(DNSEP)在法医鉴定中的应用价值。方法选取15例确诊勃起功能障碍(erectile dysfunction,ED)患者与13例正常人进行回顾性分析。结果 ED患者P40、N50及P60潜伏期延长、P40波幅下降,与正常对照组比较差异有显著性意义(P0.05)。结论阴茎体感诱发电位能较为客观地评价受检者是否存在阴茎勃起的神经通路损伤,可作为法医鉴定的辅助检查手段。     

A case of fatal intoxication with ammonium sulfate and a toxicological study using rabbits.

Agricultural fertilizers such as ammonium sulfate are widely used in house gardens as well as in agriculture, but few case reports or toxicological studies of ingested fertilizers have been reported. This paper investigates a fatal case of ammonium sulfate poisoning and demonstrates its clinical and biochemical findings in rabbits. An 85-year-old woman was found dead lying on the ground outside her house in the middle of March, but the autopsy could not determine the cause of her death. Examination at the police laboratory of the solution in the beer can found next to her showed that it was very likely ammonium sulfate. Our measurement showed a significant increase of ammonium and sulfate ions in serum and gastric contents. The cause of her death was determined as poisoning by ammonium sulfate. The total dose of 1500 mg/kg of ammonium sulfate was administered to three rabbits, all of which showed similar symptoms such as mydriasis, irregular respiratory rhythms, local and general convulsions, until they fell into respiratory failure with cardiac arrest. EEG showed slow, suppressive waves and high-amplitude slowing wave pattern, which is generally observed clinically in hyperammonemia in man and animal. There was a remarkable increase in the concentration of ammonium ion and inorganic sulfate ion in serum, and blood gas analysis showed severe metabolic acidosis. These results, mainly findings by EEG, have shown that a rapid increase in ammonium ions in blood can cause damaging the central nervous system without microscopic change. When the cause of death can not be determined, measurement of ammonium ion, inorganic ion and electrolytes in blood as well as in stomach contents at forensic autopsy is necessary.     

The course of respiration and circulation in 'toluene-sniffing'

To investigate the course of respiration and circulation in death by toluene inhalation, 25 dogs were allowed to rebreathe toluene vapor in a 1-1 plastic bag expanded with air, and electrocardiogram (ECG), electroencephalogram (EEG), blood pressure (BP) in the femoral artery and intrathoracic pressure (ITP) were registered. The respiratory movement continued two times longer than that of death by suffocation using a plastic bag of the same size. In the ECG, low voltage of R waves precipitously appeared several minutes after the beginning of the experiment and continued. The BP gradually reduced by half and kept the level for several minutes. The stage was considered toluene narcosis. Toward the end of the respiratory movement, the BP increased gradually. The analysis of the ECG complexes during the toluene inhalation revealed the direct effect of toluene to the septal and ventricular muscle of the heart. But in the end of the respiratory movement, it revealed ST segment elevation and upright T. In a few experimental animals, some of the transient arrhythmia with fluctuation of the BP appeared during the course, and in one of these dogs, fatal ventricular fibrillation occurred suddenly. These findings suggested that in most cases of sudden death in 'toluene-sniffing', the cause of death is severe hypoxia during toluene narcosis, but in a few cases, it is fatal arrhythmia due to the direct effect of toluene to the heart muscle.     

电击伤最佳病理取材部位的初步研究

目的探讨日常低电压电击后机体电流通路上极向化等病变规律和最佳病理取材部位。方法SD大鼠随机分为电击组和对照组,建立左前爪-右后爪路径220V电击大鼠模型,取电极接触处皮肤、四肢血管、神经和周边组织及腹腔大血管,常规HE染色病理组织学图像分析。结果电极接触处皮肤基底细胞(skinbasalcell,SBC)核明显极向化改变,长/短径比值与对照组比较差异高度显著,P<0.001;电流通路上腕和踝部血管及腹主动脉内皮、平滑肌细胞核的极向化与对照组比较,差异显著,P<0.05,其中腕和踝部病理改变最明显;周围骨骼肌细胞核的长/短径比值无明显规律性。结论在电击死中最常见的“手-足通路”,腕、踝部血管可能为病理取材的最佳部位。同时,由于腕和踝部距离手脚掌较远,直接接触热源和化学试剂等其他可能引起“极向化”改变的因素机会少,因此,腕和踝部血管及其周边组织的极向化改变更具有电损伤的特异性。