Morphological findings of 'cardiac concussion' due to experimental blunt impact to the precordial region.

The dog's precordial region at the sternum was impacted with a mechanical elastic-cord propelled impactor at the velocity of 8.0 m/s. The left and right intraventricular pressures and electrocardiogram (ECG) were monitored continuously for 60 min after the impact. The micro- and ultra-structure of myocardium were examined. Localization of myocardial myoglobin (Mb), creatine kinase BB (CK-BB) and creatine kinase MM (CK-MM) as well as plasma membrane permeability were studied by immunohistochemical and lanthanum probe techniques. Upon the impact, abrupt over-pressures within both ventricles were recorded with transient depression of the left ventricular systolic pressure. In all the dogs, some rhythm- and conduction-disorders were noted, which lasted transiently and resumed to normal sinus rhythm. At autopsy, no gross injuries of the heart were detected, and microscopic examination showed no visible myocardial lesions. However, immunohistochemically, focal patchy loss of myocardial Mb, CK-BB and CK-MM was identified with scattered deposition of these substances between myocardial fibers elsewhere. Such changes as relaxed myofibrils with widened I band, contracted myofibrils and broken cristae of the mitochondria were observed in myocardial ultrastructure. Lanthanum particles deposited inside the mitochondria. These results indicate that increase in cardiac cell membrane permeability and ultrastructural damage in myocardium may be involved even in cardiac concussion.     

Morphological findings of ‘cardiac concussion’ due to experimental blunt impact to the precordial region

The dog’s precordial region at the sternum was impacted with a mechanical elastic-cord propelled impactor at the velocity of 8.0 m/s. The left and right intraventricular pressures and electrocardiogram (ECG) were monitored continuously for 60 min after the impact. The micro- and ultra-structure of myocardium were examined. Localization of myocardial myoglobin (Mb), creatine kinase BB (CK-BB) and creatine kinase MM (CK-MM) as well as plasma membrane permeability were studied by immunohistochemical and lanthanum probe techniques. Upon the impact, abrupt over-pressures within both ventricles were recorded with transient depression of the left ventricular systolic pressure. In all the dogs, some rhythm- and conduction-disorders were noted, which lasted transiently and resumed to normal sinus rhythm. At autopsy, no gross injuries of the heart were detected, and microscopic examination showed no visible myocardial lesions. However, immunohistochemically, focal patchy loss of myocardial Mb, CK-BB and CK-MM was identified with scattered deposition of these substances between myocardial fibers elsewhere. Such changes as relaxed myofibrils with widened I band, contracted myofibrils and broken cristae of the mitochondria were observed in myocardial ultrastructure. Lanthanum particles deposited inside the mitochondria. These results indicate that increase in cardiac cell membrane permeability and ultrastructural damage in myocardium may be involved even in cardiac concussion.     

早期心肌挫伤超微结构变化的实验研究

应用机械式弹性拉力打击器以10.0米／秒速度冲击犬胸骨心前区，引起心肌挫伤。分别对伤后2～5min、30～60min、3h及5h心肌挫伤区超微结构变化进行观察。结果显示：（1）伤后2～5min即见严重的心肌超微结构损害，如肌原纤维撕裂、扭曲变形，肌节过度收缩或I带增宽Z线弯曲、线粒体破裂，部分嵴不清、间质出血并可见游离的线粒体。伤后30～60分钟挫伤心肌肌原纤维溶解、碎裂，线粒体破裂伴嵴消失。伤后3及5h，挫伤区坏死明显，坏死物与红细胞碎片混杂一起，结构不能辨认。（2）同一心脏可有多部位损伤，且损伤程度不均一。     

实验性心脏震荡的法医病理学研究

本研究应用可产生稳定打击速度并可同时测定瞬间冲击速度及冲击力大小的机械式弹性拉力打击器，分别以６．７ｍ／ｓ及８．０ｍ／ｓ速度冲击大胸骨部心前区建立了心脏震荡动物模型，在左右心室压力及心电图监测下冲击后６０分钟进行尸体剖验检查，并应用多种组织化学染色、透射电镜技术、免疫组织化学染色以及硝酸镧示踪电镜技术对心肌组织学行系统性研究。结果表明：１．心前区受冲击瞬间左右心室内压力急骤升高，随即可恢复至正常水平。心电图在冲击后即刻表现为持续短暂的异常心律，逐渐恢复至正常心律。２．心脏血管麻痹性扩张，但宏观及微观均无损伤性所见。３．心肌超微结构有一定程度损害，心肝细胞膜破裂或通透性增高。本研究提示：心脏震荡者心脏宏观、微观无特殊改变，但超结构及心肌细胞膜轻度损害。     

实验性早期心肌挫伤的免疫组织化学研究

应用机械式弹性拉力打击器，以10．0m／s速度冲击犬胸骨心前区，建立免疫组织化学染色对伤后2～5分钟、30～60分钟、3小时及5小时心肌挫伤组织中Mb、CK－BB及CK－MM的变化进行观察。结果表明：（1）心肌挫伤后2～5分钟检出心内膜下肌层已有重度心肌Mb脱失及中度CK－BB、CK－MM脱失，并沉积于心肌纤维间，同时吸收入血。随着伤后时间延长，挫伤区三种物质脱失加重，但间质中沉积量减少乃至消失；（2）波浪变心肌中也可见三种物质的轻度脱失；（3）同一心脏中不同部位心肌的损伤程度不同、证明应用免疫组织化学染色技术可发现心肌挫伤性损害。心前区受到相当程度的钝力冲击后心脏不同部位损害程度不同。     

实验性心脏挫伤动物模型的建立

本研究应用自制机械式弹性拉力打击器以9．1～10．5m／s速度冲击动物胸骨心前区，不仅导致左右心室压力、心电图及心率发生改变，而且造成了心脏挫伤等宏观的病理形态学变化，成功地建立了心脏挫伤动物模型，为深入研究钝力性心脏外伤奠定了基础。     

肌红蛋白诊断早期心肌梗死的特异性研究

目的　探讨肌红蛋白在早期心肌梗死死后诊断的特异性。方法　应用免疫组织化学S -P法检测梗死心肌和其它非梗死性的直接或间接心肌损害的心肌肌红蛋白染色的变化。结果　梗死心肌均可见不同程度的肌红蛋白缺染 ,其它非梗死性的直接或间接心肌损害的心肌中 ,如心脏挫伤、心肌炎、出血性休克、电击死、机械性窒息、有机磷中毒等 ,也有不同程度的肌红蛋白缺染。结论　应用肌红蛋白免疫组织化学方法诊断早期心肌梗死需慎重     

多发性软组织挫伤后对肺及其他脏器的影响

目的观察多发性软组织挫伤后短时间内死亡案例的脏器病理学改变。方法应用常规组织学及免疫组织化学染色技术进行光学显微镜检查。结果光镜检查见肺组织毛细血管扩张充血，白细胞集聚，肺组织散在片状出血、灶状坏死及透明膜形成；心脏间质血管扩张充血，点灶状纤维溶解；脑组织充血水肿，肝脾充血。免疫组化发现肺泡腔及部分血管内纤维蛋白染色阳性，部分脾脏血管内及肾髓质集合管中肌红蛋白染色阳性。结论本研究结果提示多发性软组织挫伤后短时间内死亡的死因为成人呼吸窘迫综合征（ARDS）合并多脏器功能衰竭。     

28例心脏挫伤的法医病理学观察

目的观察心脏挫伤的形态特点和分布规律,探讨心脏挫伤的分类和分级方法及与成伤机制的关系。方法用改良的心脏挫伤检查法对28例人体心脏挫伤标本进行肉眼和光镜观察并测量挫伤灶的大小。结果肉眼观察,心脏挫伤灶切面一般呈带状、楔形、类圆形或条纹状;观察连续切面,可见其相应的三维形态大致呈类圆盘状、类圆锥体、类球体或线状。显微镜下,挫伤区主要表现为轻重不等的出血、心肌纤维断裂和心肌细胞变性坏死,按出血和变性坏死的程度可将心脏挫伤分为出血型、坏死型和出血坏死型。心脏挫伤见于心脏各部位和心壁各层,不同部位的挫伤发生率和类型差异大。以挫伤灶的体积、数量和部位为依据,将心脏挫伤的程度分为4级。结论心脏挫伤的形态多样、分布广泛、各部位的挫伤类型和发生率差异大。     

Diagnostic efficacy of biochemical markers in diagnosis post-mortem of ischaemic heart disease

In forensic medicine, there is a need for more sensitive biochemical markers for the post-mortem diagnosis of acute myocardial infarction. A study of the distribution of biochemical markers in different fluids is of great significance in post-mortem diagnosis, because their distribution depends on the location of tissue damage and release kinetics. The aim of this study is to compare the sensitivities and specificities of creatine kinase-MB (CK-MB), myoglobin and cTnI in serum and pericardial fluid for the post-mortem diagnosis of acute myocardial infarction (AMI). We studied 188 cadavers selected during 1 year from medicolegal autopsies. The groups were as follows: (1) myocardial infarction (n = 52); (2) asphyxia (n = 59); (3) multiple trauma (n = 41); (4) natural deaths excluding myocardial infarction (n = 36). We obtained statistically significant differences in pericardial fluid for all the biochemical markers, the highest levels being obtained in the group of cadavers who had died from myocardial infarction. A common factor is the high negative predictive value found in biochemical markers, which is contrary to the findings obtained in clinical practice, when the percentages of sensitivity are very high.     

钝力冲击后心脏组织形态学变化的实验研究

本研究用自制机械式弹性拉力打击器以６．７ｍ／ｓ、８．０ｍ／ｓ、９．１ｍ／ｓ及１０．０ｍ／ｓ速度冲击大胸骨心前区，然后采用多种组织学染色及透射电镜技术对心脏组织形态学变化进行了观察。结果表明：①以６．７ｍ／ｓ及８．０ｍ／ｓ速度冲击后心脏宏观未见有明显改变，微观可见心肌波浪变。电镜下可见肌原纤维肌节收缩，Ｉ带消失或轻度Ｉ带增宽乃至肌原纤维断裂。②以９．１ｍ／ｓ及１０．０ｍ／ｓ速度冲击后宏观可见心脏挫伤，微观心肌挫伤改变明显，实验观察６０ｍｉｎ内心肌血管内皮损伤处已有血小板粘附集聚甚至血栓形成，心肌超微结构损害严重。③同一心脏可有多部位损伤，且损伤程度不均一。本研究进一步表明钝力性心脏外伤中．虽然无宏观损伤所见，其微观，特别是超微结构可有损害。     

Sudden cardiac death: a comparative study of morphological, histochemical and biochemical methods.

The study deals with the comparison of morphological, histochemical and biochemical methods applied to the detection of myocardial infarction in 150 medico-legal autopsies performed at the Institute of Forensic Pathology in Copenhagen. The study also included an NBT (formazan) test of cardiac cross-sections, and light microscopy and fluorescence microscopy of acridine orange-stained specimens from four different sites of the cardiac musculature. Specimens of myocardium from the same four sites and pericardial fluid were analysed biochemically at the Institute of Legal Medicine in Granada. The K+/Na+ ratio was determined in the myocardial tissue and total creatine phosphokinase activity, creatine phosphokinase isoenzymes (MM, MB and BB) and myoglobin were assayed in pericardial fluid. When the results from Copenhagen and Granada were compared, there was absolute concordance in 96 cases, discrepancy in 53 and one case was inconclusive. After studying the circumstances of death, the number of discrepancies were reduced to 20, so that concordance was reached in 86% of all the cases. The results show that the combination of different methods leads to a diagnosis of myocardial infarction in far more cases than with morphological or biochemical methods alone.     

常用心脏标志物的生化检测及法医学应用

在法医病理学鉴定工作中,由早期缺血性心肌病变及致死性心律失常引起的心源性猝死常常缺乏典型的病理组织学改变,如何准确、客观地诊断、查明死因是法医病理学亟待解决的问题。近来研究发现的一些心肌特异性指标对心源性猝死的诊断有很好的应用前景。本文介绍几种常见心肌特异性标志物的生化特点、实验室检验方法以及临床和法医学应用前景,以期为心源性猝死的法医病理学鉴定提供依据。     

纤维蛋白原在心肌梗死死后诊断的特异性研究

为探讨纤维蛋白原(Fg)在心肌梗死死后诊断的特异性,应用免疫组织化学和图像分析技术,对正常心脏、心肌梗死及其它非梗死性的引起直接或间接心脏损害的情况如心肌炎、窒息、电击死、出血性休克、心挫伤、有机磷中毒等心肌细胞内Fg的变化进行研究。结果发现:正常对照组心肌细胞内未见Fg阳性反应,而心肌梗死、心肌炎、窒息、电击、休克、心挫伤、有机磷中毒等组均可见Fg阳性反应,且各组Fg阳性反应面积与正常对照组存在显著性差异。因此Fg作为心肌梗死死后诊断指标,易受心肌炎、窒息、电击、休克、心挫伤、有机磷中毒等的影响,对诊断心肌梗死的特异性较差。     

The relevance of the detection of troponins to the forensic diagnosis of cardiac contusion

The forensic diagnosis of cardiac contusion has hitherto been based mainly on anamnesis, concomitant thoracic injuries and the detection of macroscopic changes to the heart. Parallel histological and serological investigations of the heart-specific troponins have been conducted with varying results. This paper aims to show whether heart-specific troponins are suitable as a means of securing the diagnosis in proven cases of cardiac contusion and of determining which of the three heart-specific troponins cTnT, cTnI and cTnC are most significant in serology and histology for postmortem diagnosis. In the study, 25 cases of known cardiac contusion and 11 controls without vital myocardial trauma taken from autopsy material were prospectively investigated. Investigation of the venous serum revealed significant differences in the concentrations of the case and control groups for troponin T (mean value 5.5056 versus 0.4982; p=0.014), for troponin C (mean value 263.9280 versus 68.5640; p=0.001) and for troponin I (mean value 1404.0560 versus 36.1650; p=0.003). In histology there are also significantly different depletions between the groups investigated (cTnT: p=0.002; cTnC: p=0.003; cTnI: p<0.001) taking into account the autolysis time.     

电击后心脏损伤的实验研究

将电击器电路连接家兔左前肢和右后肢，用200v5mA交流电定时电击，制造电击死和电击伤时心脏损伤的动物模型。结果显示：电击死前ECG出现室颤波，光镜下心肌纤维广泛断裂，间质出血，小血管周围水肿．心肌灶性坏死，心房心肌坏死累及心内膜时有微小附壁血栓形成；房室结细胞核空泡变，胞浆深嗜伊红性；电镜下心肌纤维闰盘撕裂；心肌Ⅰ带消失，肌节缩短，超收缩带（Hypercontractionbands）形成，或Ⅰ带扩大，肌节拉长，Z线移位；肌原纤维溶解等。电击伤动物出现心肌散在性坏死灶内炎性浸润，灶性心内膜炎，小冠状动脉狭窄或闭塞。传导系统炎性浸润。本实验对电击死的法医学鉴定和非致死性电击伤心脏并发症的诊断提供病理学基础。     

补体C_5在心肌梗死死后诊断的特异性研究

为了探讨补体 C5在心肌梗死死后诊断的特异性,应用免疫组织化学和图像分析技术 ,对正常心脏、心肌梗死及其它非梗死性的引起直接或间接心脏损害的情况如心肌炎、窒息、电击死、出血性休克、心挫伤、有机磷中毒等心肌细胞内 C5的变化进行研究。结果发现： C5仅在心肌梗死与心肌炎病例出现阳性反应,其阳性反应面积同正常对照组存在显著性差异,在窒息、电击死、出血性休克、心挫伤、有机磷中毒等病例未见明显阳性反应。因此 C5作为心肌梗死死后诊断指标仅受心肌炎的影响,对诊断心肌梗死具有较好的特异性。     

纤维连接蛋白在诊断心肌梗死的特异性研究

探讨纤维连接蛋白 (Fn)对心肌梗死死后诊断的特异性。应用免疫组织化学和图像分析技术 ,对正常心脏、心肌梗死及其它非梗死性因素 ,如心肌炎、窒息、电击死、出血性休克、心挫伤、有机磷中毒等 ,直接或间接引起心脏损害时心肌细胞内Fn的变化进行研究。结果发现 :Fn仅在心肌梗死与心肌炎病例出现阳性反应 ,其阳性反应面积同正常对照组存在显著性差异 ,在窒息、电击死、出血性休克、心挫伤、有机磷中毒等病例未见明显阳性反应。Fn作为心肌梗死死后诊断指标仅受心肌炎的影响 ,对诊断心肌梗死具有较好的特异性     

补体C5在心肌梗死死后诊断的特异性研究

为了探讨补体C