大鼠急性斑蝥中毒血流动力学研究

大鼠急性斑蝥中毒的血流动力学研究结果显示,灌胃后,大鼠左心室舒张末压(LVEDP)呈下降趋势,左心室内压(LVP)和左室压最大变化速率(±dp/dt max)变化不明显;心率(HR)在低剂量组加快,而大剂量组减慢;心电图(EKG)无明显改变;呼吸频率(RR)先快后慢,大鼠死亡时,呼吸比心跳早停止几分钟。提示斑蝥中毒死亡较快时,呼吸抑制作用是一个不容忽视的因素。     

乌头生物碱及其代谢物在家兔死后体内分布研究

目的研究乌头生物碱及6种代谢物在中毒家兔死后体内的分布规律,为乌头生物碱中毒案件中检材的选取提供参考依据。方法将生川乌粉碎制成水煎剂,以其中乌头碱的LD50计算,给予家兔灌胃,待其死亡后立即解剖取材,采用高效液相色谱-串联质谱测定检材中乌头生物碱及6种代谢物的含量。结果乌头生物碱及6种代谢物在各脏器及体液中的死后分布情况为:(1)乌头碱:尿液外周血、心血、胃、肺、肾、心、肝、肌、脾;(2)新乌头碱:尿液外周血、心血、肺、胃、肾、肝、肌、脾、心;(3)次乌头碱:尿液外周血、心血、胃、肺、肝、脾、肾、肌、心;(4)苯甲酰乌头原碱:尿液外周血心血胃、脾、肾、肺、肌、心、肝;(5)苯甲酰新乌头原碱:尿液外周血心血胃、脾、肾、肺、肌、肝、心;(6)苯甲酰次乌头原碱:尿液外周血心血、胃、肾、脾、肺、肌、肝、心;(7)乌头原碱:尿液外周血、心血、肾、胃、心、脾、肝、肌、肺;(8)新乌头原碱:尿液外周血、心血、肾、胃、肝、心、肺、脾、肌;(9)次乌头原碱:尿液外周血、心血、肝、肾、脾、胃、心、肺、肌。结论乌头生物碱及6种代谢物分布以血液和尿液中为主,在脏器以胃、肺脏、肾脏和肝脏等含量较高。     

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。     

限制性体位引起肺动脉血栓栓塞2例

<正>1案例1.1案例1姜某,男,49岁,在押期间于某日凌晨因情绪不稳加戴戒具,早晨6:00许解除戒具,上午10:00许在转移过程中突然晕倒,抢救无效后死亡。尸体检验:心腔内血液不凝,呈流动性。心内膜及各瓣膜光滑,主动脉根部散在粥样硬化斑块形成,冠状动脉左前降支及右冠状动脉管腔Ⅰ~Ⅱ级狭窄。双肺苍白,含气丰富。剪开肺动脉及其左、右分支,见左、右肺动脉末端及肺叶肺动脉内有血栓栓塞,以右肺叶     

先天性主动脉-肺动脉间隔缺损1例

主动脉-肺动脉间隔缺损(aortopulmonaryseptalde鄄fect)又称主动脉-肺动脉窗或主-肺动脉瘘,为一种罕见的先天性心脏病。我们遇见1例因新生儿死于该疾病而引发医疗纠纷的案件,报道如下。1案例妊娠足月剖宫产,男性新生儿,体重2600g。出生后,全身轻度紫绀,未闻及心脏杂音、肺湿罗音;四肢活动无力。Apgar评分:1min6分;5min7分。临床诊断:新生儿呼吸窘迫综合征?经救治,症状不见好转。出生后5h,突然呼吸急促,全身紫绀明显,心底部闻及收缩期杂音、肺湿罗音,死亡。尸检所见:死后48h尸检。尸长48cm,发育正常、营养中等,体表未见明显畸形。尸斑暗红色…     

两种窒息死亡方式下大鼠体内缺氧诱导因子1-α的变化规律

目的探讨氮气处理窒息死及缢死后大鼠心、肝、肺、肾中缺氧诱导因子1-α(HIF1-)α的表达变化规律及法医学意义。方法制作大鼠氮气处理窒息死及缢死两种窒息模型,记录其特征表现;应用免疫组织化学方法及图像分析技术测定大鼠窒息死后不同时间段HIF1-α在心肌、肺、肝、肾中的分布变化;结果HIF1-α表达于两种窒息模型的心肌细胞、肝细胞、肾小管细胞以及肺部各种细胞,各时间段的窒息组和对照组HIF1-α的表达有明显区别;氮气处理窒息死组四种组织在死亡后0、6和24h表达有减弱趋势,0h有核阳性表达,呼吸及心跳停止时间比缢死组短,各组织表达阳性率比缢死组稍弱;缢死组在除心肌表达逐渐增强外其他组织表达在6h出现一个表达高峰(此时核阳性表达最多),后表达逐渐减弱;对照组表达平稳,均未见到核阳性。结论在死亡后24h内检测组织中HIF1-α的表达可以作为推断窒息死的一个生物学指标。     

家兔双前肢悬挂致死过程中的电生理研究

目的探讨悬挂体位致窒息死亡的电生理方面的机制。方法成年家兔12只,雌雄不限。随机分为两组:一组监测膈肌肌电图,另一组监测肋间肌肌电图、心电图、脑电图。取仰卧位固定,手术暴露膈肌和肋间肌,引导肌电图;同时引导标准Ⅱ导联心电图和脑电图。然后将家兔固定双前肢悬挂,连续监测实验过程中家兔的心电、脑电、肌电图的变化情况,直至其死亡。结果悬挂末期和悬挂初期相比,膈肌肌电频率下降(P<0.05)、呼吸波持续时间、振幅和面积均有延长或增多(P<0.05)、最大传导速度无变化;肋间肌仅见肌电频率下降(P<0.05);脑电振幅降低(P<0.01)、δ波增多(P<0.01)、β波减少(P<0.05);心电仅见各波形振幅的降低(P<0.01)。膈肌肌电频率的下降最早,脑电频率的下降次之,肋间肌肌电的下降最晚(P<0.01)。结论悬挂体位致窒息死亡的机制的始动因素是呼吸运动受限,并最终形成外周性呼吸肌疲劳和呼吸中枢缺氧性衰竭而发生死亡。     

成人非典型急性流脑猝死1例

随着抗生素的广泛使用 ,流行性脑膜炎的发病死亡率已经很低 ,而成人患此病死亡则更罕见 ,[1] 现报道一例 :某男 ,2 6岁。某日被人发现死亡 ,死亡前一天因头痛、头昏、发烧、咽痛到某医院门诊就诊。家属怀疑死亡与临床用药有关 ,要求尸检确定死亡原因。尸检发现 :死者发育正常 ,营养中等 ,颜面部及躯干、四肢皮肤点状或片状出血 ,大小为针头大至 1.5ｃｍ× 1.5ｃｍ ,双眼睑结膜下出血点。左肺 5 5 0 ｇ ,右肺 6 2 0 ｇ ,双肺表面可见出血斑 ,切面未见结节及空洞。心包腔见少量液体 ,心 330ｇ ,心包膜可见出血点 ,冠状动脉及心瓣膜未见明显异…     

类胰蛋白酶在过敏性休克死者心肺肠组织中的表达

目的观察过敏性休克死亡者心、肺及空肠组织中类胰蛋白酶免疫荧光表达的强度,为过敏性休克死亡提供法医学鉴定依据。方法运用免疫荧光染色法对过敏性休克死亡者心、肺及空肠组织进行类胰蛋白酶染色,荧光显微镜观察并采集图像,Image-pro plus6.2软件进行图像分析并计算阳性颗粒数,运用SPSS17.0软件进行统计学分析。结果过敏性休克死亡者心、肺及空肠组织中类胰蛋白酶的表达均明显高于对照组(P0.05),其差异具有统计学意义。结论当高度怀疑过敏性休克但无法获得满意的血液标本时,检测其心、肺及空肠组织中类胰蛋白酶的免疫表达可作为过敏性休克死亡法医学鉴定的辅助手段。     

26例肺动脉血栓栓塞的法医学分析

肺动脉血栓栓塞,简称肺血栓栓塞（pulmonary thromboembolism PTE）,指血栓物质随血流进入肺动脉主干及其分支堵塞血管,造成急性肺循环障碍及心功能障碍。PTE发病急速,症状不典型,     

固定双上肢悬挂致死的SOD,MDA含量变化

固定双上肢将身体悬空致死，是一种罕见的、特殊的窒息死。实验结果表明：实验后与实验前相比，ＳＯＤ活性明显下降，有显著性差异（Ｐ＜０．０１），ＭＤＡ含量明显升高，有显著性差异（Ｐ＜０．０１）。这为进一步阐明这类固定双上肢将身体悬空所致的死亡为窒息死，为法医学鉴定提供科学的依据。     

The course of respiration in death caused by obstructive asphyxia

Experiments were carried out on 30 dogs to investigate the course of respiration during obstructive asphyxia. They were asphyxiated by occlusion of the exposed trachea. Intrathoracic pressure, blood pressure in the femoral artery, electrocardiogram and electroencephalogram readings were registered. In most cases, the respiration course during the dyspnea stage by occlusion of the trachea generally had an inspiratory character. In a few animals, when the trachea was occluded in the expiratory phase, there were a few positive expiratory respirations with moderate inspiratory movement and thereafter the respirations were inspiratory during the dyspnea stage. The terminal respirations, which occurred 1-2 min before the circulatory breakdown, were generally inspiratory, but in a few dogs they were expiratory.     

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.     

The course of respiration and circulation in death by carbon dioxide poisoning

To investigate the effects of very high concentrations of carbon dioxide (CO2) upon the course of respiration and circulation, dogs were allowed to breathe high concentrations of CO2 while intrathoracic pressure, blood pressure (BP) in the femoral artery, electrocardiogram and electroencephalogram readings were registered. The respiratory movements either increased just after inhalation of high concentrations of CO2 and then ceased in 1 min, or decreased and continued for a while according to the concentrations of CO2. The BP showed an initial depression, then returned to the original level, then fell again rapidly or maintained an appreciable level for a while until circulatory breakdown. In the dogs allowed to breathe the gas mixture of 80% CO2 with 20% O2, the respiratory movement ceased in 1 min, and the terminal respirations were seen with the circulatory breakdown after apnoea of several minutes. These findings showed that the cause of death in breathing high concentrations of CO2 is not hypoxia, but the CO2 poisoning.     

Cardiac Inhibitory Reflex as a Cause/Mechanism of Death

The role of cardiac inhibitory reflex as a potential cause of death is still a matter of debate. This study reports two cases of death under unusual circumstances. Case 1 corresponds to a man found hanging where the role of ligature compression of the carotid sinus became relevant as a possible explanation of death. In Case 2, the participation of a vasovagal syncope was clearly triggered by the laryngoscopic procedure. It is proposed that cardiac inhibitory reflex should be taken into account in those cases of unexpected death, which fulfills the following three criteria: (i) The investigation of the circumstances of the death is consistent with a hypothesis of cardiac arrest. (ii) A typical triggering peripheral stimulus is present. (iii) The performance of a complete autopsy cannot rule out the participation of a cardiac inhibitory reflex in the cause of death.     

Cardiac arrest after traffic accident induced through vagal reflex in a case with bilateral stenosis of vertebral arteries

An 84-year-old driver suffered cardiac arrest after a traffic accident. He was quickly resuscitated and transferred to a hospital where he was treated in a state of unconsciousness and respiratory failure for 20 days until his death. The brain stem was rendered anoxic during cardiac arrest, which caused the respiratory failure. Artificial ventilation and catecholamine infusion were carried out, resulting in myocardial degeneration. Bilateral stenosis of the vertebral arteries was disclosed, but no injuries or hemorrhage of the brain and spinal cord were detected. On days 3 and 4 after admission, immediately after the head of the victim was flexed forward for examinations, cardiac arrest was induced twice, but was controlled either by administering atropine or by restoring the original posture. Positional change is known to induce vagal reflex that results in bradycardia, hypotension or cardiac arrest in sensitive persons. The victim might have undergone the reflex-mediated cardiac arrest after the accident, to which the stenosis of the vertebral arteries may have contributed.     

Hanging: fulminant thrombembolia as a vital reaction? (author's transl)]

Fulminant pulmonary thrombembolias were found in two suicides committed by hanging. The origin was a thrombosis of the iliac vein in one case and of femoral veins in the other. The thrombi and emboli respectively were examined histologically. It is assumed that the detachment of the emboli might have been caused mechanically during terminal muscle-cramps or hemodynamically by sudden alterations of blood pressure.     

Drowning without aspiration: is this an appropriate diagnosis?

It has been reported that 10-15% of drowning victims do not aspirate water. We have revisited the original studies quoted to reach this conclusion and find it is without foundation. Sudden cardiac standstill is known to occur on land and, therefore, may also occur when the victim is in water. In the absence of the common finding of significant pulmonary edema in the victim's respiratory system, to conclude his or her death was caused by "drowning without aspiration" is unwise. All causes of sudden death that might occur in which respiration may not take place should receive serious consideration when examining bodies with such findings that are found in water.     

Widespread myocardial and pulmonary bone marrow embolism following cardiac massage.

Widespread fatal massive bone marrow embolism of the coronary and the pulmonary arteries are described in a 71-year-old man with a respiratory disease. Cardiac massage was carried out during the cardiac arrest. In autopsy findings there were no fractures of the ribs or the sternum. The authors suggested that the cardiac massage was the most important predisposing factor for the bone marrow embolism.     

Sudden Death Caused by Anomalous Origin of the Coronary Artery During Exercise

Anomalous origin of the coronary artery (AOCA) is a rare, but important cause of sudden cardiac death among young athletes. Nine autopsy cases (8 male, 1 female; mean age, 17.9 years; age range, 11–31 years) of sudden death during or just after exercise caused by AOCA were reviewed. The exercises performed at the time of death were running (4 cases), soccer (2 cases), and baseball, swimming and kendo (Japanese swordsmanship) (1 case each). In 6 cases, the left coronary artery arose from the right sinus of Valsalva, and in 3, the right coronary artery from the left sinus. The coronary arteries passed between the pulmonary artery and the aorta with an acute angle takeoff from the orifice. Three cases had cardiovascular manifestations prior to death. In cases with cardiovascular manifestations, novel imaging methods should be considered to prevent sudden death.