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.     

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。     

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。     

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     

Efficacy of cerebro-spinal fluid biochemistry in the diagnosis of brain insult.

Postmortem biochemical indices may provide a useful adjunct to morphological studies in the identification of antemortem brain insult. We studied 34 routine medico-legal cases categorising them into one of four diagnostic groups. There were 11 cases of head trauma, 7 of 'hypoxia' (3 hangings and 4 carbon monoxide or drug poisonings), 7 sudden cardiac deaths and 9 miscellaneous cases. Survival time and postmortem interval was known for each case. The degree of cranio-cerebral trauma was graded. Cerebro-spinal fluid (CSF) and vitreous humour were analysed for calcium, glucose, total proteins, aldolase, aspartate transaminase (AST), alanine transaminase (ALT), gamma glutamyltransferase (GGT), lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase BB isoenzyme (CK-BB). CK-BB was also measured in superior vena cava serum. In CSF there was a significant correlation between the severity of cranio-cerebral trauma and levels of aldolase, CK-BB, AST, ALT and total proteins. CSF CK-BB, median units/l (range), for the groupings of head trauma, hypoxia, sudden cardiac death and miscellaneous were respectively 823 (2-3431); 96 (2-187); 4 (2-25); 5 (1-69). Corresponding serum CK-BB levels were 240 (28-322); 390 (26-411); 180 (20-482); 79 (18-530).     

Diverse morphological lesions and serious arrhythmias with hemodynamic insults occur in the early myocardial contusion due to blunt impact in dogs

To investigate the morphology and hemodynamics of the early myocardial contusion, an animal model of cardiac contusion was established by impact to the precordial region at sternum at velocity of 10.0m/s with a mechanical elastic-cord propelled impactor in 19 dogs. The electrocardiogram and both the left and right intra-ventricular pressures were recorded continuously throughout the experiment. Histological and immunohistochemical examinations of myoglobin, creatine kinase-MB and fibrinogen were conducted. At the moment of impact, abrupt over-pressures within the left and right ventricles occurred with concomitant serious arrhythmias followed by variety of cardiac conduction disorders and depressed left and right ventricular systolic pressures during the observation times. Histologically, lesions of myocardial contusions were identified at subepicardial, myocardial or subendocardial layer as interstitial hemorrhage, disruption or coagulative necrosis as well as contraction band necrosis of the muscle fibers, which might be categorized into the hemorrhagic, necrotized and mixed forms. The three forms of lesions were found to exist independently, or co-existed in a heart. However, severity of the lesions varied greatly with different parts even within a heart. Intravascular thromboses were occasionally discovered post-impact. Immunohistochemically, loss of myoglobin and creatine kinase-MB from cardiac cells, and accumulation of fibrinogen at the cell membranes were detected 5min post-impact. The intracellular accumulation of fibrinogen increased with extension of post-impact intervals. Our results indicate that diverse morphological lesions concomitant with hemodynamic compromise and serious, even fatal arrhythmias occur in the early myocardial contusion, and intravascular thromboses are occasionally produced, suggesting that traumatic myocardial ischemic lesion may be induced due to blunt impact to the precordial region.     

失血即刻死亡心肌超微结构,组织化学及免疫组化研究

本研究应用电镜、组织化学、免疫组化及形态计量分析等方法和技术，观察失血即刻死亡时家兔心肌超微结构、琥珀酸脱氢酶（ＳＤＨ）活性、肌红蛋白（Ｍｂ）脱失的变化特点。结果发现，失血即刻死亡时家兔心肌细胞轻度水肿，肌原纤维普遍强度收缩，肌节缩短，Ｚ线增粗，心肌细胞内ＳＤＨ活性明显下降，Ｍｂ轻度局灶性脱失．     

云南不明原因猝死地区隐花青鹅膏的毒性研究

目的 探究云南不明原因猝死案件事发当地隐花青鹅膏的毒性及毒理机制.方法 采集事发地的隐花青鹅膏,经基因测序鉴定种属后制成干粉和熬煮物,SD大鼠灌胃染毒,提血清测定肝、肾功能以及心肌酶谱的生化指标.灌胃染毒7次后,取大鼠心肌、肝脏和肾脏组织进行HE染色和透射电镜观察.最后运用SPSS 21.0统计学软件分析数据.结果 高...     

An autopsy case of neuroleptic malignant syndrome (NMS) and its immunohistochemical findings of muscle-associated proteins and mitochondria

Neuroleptic malignant syndrome (NMS) is a rare but potentially fatal disorder. In forensic cases, post-mortem diagnosis of NMS is sometimes difficult if ante-mortem information, such as neuroleptic ingestion or signs and symptoms, cannot be obtained. A 39-year-old Japanese male on a neuroleptic treatment regimen suddenly became agitated and died. Autopsy revealed muscle rigidity and hyperthermia. Post-mortem examination of blood revealed elevation of creatine phosphokinase-MM (CK-MM) and lactate dehydrogenase-4 and dehydrogenase-5 (LDH-4 and LDH-5). In renal glomeruli and tubules, myoglobin was stained immunohistochemically. From these findings, the cause of death was considered to be NMS. To support the diagnosis of NMS, both skeletal and cardiac muscles were stained with actin, myoglobin, desmin and mitochondria antibodies immunohistochemically. Actin, myoglobin, desmin, and mitochondria had been lost from skeletal, but not from the cardiac muscle, which suggested that only the skeletal muscle was damaged. Moreover, because mitochondria had disappeared only from the skeletal muscle, it was considered that skeletal muscle degeneration was caused by mitochondrial damage. Therefore, it is suggested that immunostaining of skeletal muscle by antibodies for muscle-associated proteins and mitochondria is useful to corroborate a diagnosis of NMS.     

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。     

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。     

心肌梗死6项免疫组化指标的死后稳定性比较

目的　探讨用于早期心肌梗死死后诊断的维连接蛋白 (Fn)、纤维蛋白原 (Fg)、补体 (C5 )、肌红蛋白(Mb)、肌动蛋白 (HHF3 5 )、结蛋白 (Dm )等 6项免疫组化指标在死后不同时间的稳定性。方法　应用免疫组织化学法、图像分析和统计学处理系统 ,检测缺血心肌细胞内Mb、HHF3 5、Dm的缺失面积和Fn、Fg、C5的阳性反应面积 ,并对 6项免疫组化指标在死后不同时间的稳定性进行比较。结果　正常心肌组织 4℃放置 1～ 2d ,Dm、HHF3 5、Mb染色均匀 ,未见明显缺失 ;放置 3d以上 ,即可见Dm、HHF3 5、Mb明显缺失 ,且随放置时间延长 ,缺失面积逐步增大。缺血心肌组织随放置时间延长 ,Dm、HHF3 5、Mb的缺失面积逐步增大 ,Fg、C5、Fn阳性反应面积逐渐减少 ;放置 14d以上 ,Fg呈阴性反应 ;放置 2 1d以上 ,C5呈阴性反应 ;放置 2 8d ,Fn仍呈阳性反应。正常心肌组织放置不同时间 ,均未见Fg、C5、Fn阳性反应。图像分析结果显示阳性反应面积逐步减少。结论　Dm、HHF3 5、Mb的稳定性最差 ,易受死后自溶的影响 ,只适用于新鲜尸体 (死后 1～ 2d) ;Fg次之 ,可用于死后 4℃放置 7d的尸体 ;C5较好 ,可用于死后 4℃放置 14d的尸体 ;Fn稳定性最好 ,可用于死后 4℃放置 2 8d的尸体。     

冠心病猝死心肌肌红蛋白缺失的免疫组化研究

作者应用免疫组化ABC法首次对SCD及对照组病例的心肌Mb缺失情况进行了研究,并经扫描显微镜光度计测量及电子计算机统计分析,结果发现SCD组心肌Mb均有明显缺失,呈现多发、散在、节段性分布,而对照组无缺失,认为这种多发、散在、节段性Mb缺失可作为无大片心肌梗死的SCD病例的诊断标志之一,为SCD的尸检诊断开辟了新途径。     

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.     

Actin、Dm、Mb和Fn诊断急性心肌梗死的研究

目的探讨Actin、Dm、Fn和Mb在诊断急性心肌梗死中是否具有实际应用价值。方法选取已确诊的30例尸检心脏标本,分为急性心肌梗死组、冠状动脉粥样硬化组及正常心肌组。在心脏左前壁取材,连续切片,分别作HE染色,Actin、Dm、Fn和Mb免疫组化SP法染色,采用图像分析技术客观测量及比较各组标本染色强度。结果在急性心肌梗死组和冠状动脉粥样硬化组中,Actin、Dm和Mb在心肌细胞中表达均明显缺失,而Fn明显表达;而且在这两组间此4项指标表达效果无统计学差异。在正常心肌组中,Actin、Dm和Mb在心肌细胞中表达均无缺失,而Fn不表达。结论Actin、Dm、Fn和Mb对心肌细胞的缺血缺氧十分敏感,能反映明确的心肌坏死,但对坏死发生的机制缺乏特异性,因此用于诊断急性心肌梗死时需慎重。     

青壮年猝死综合征心肌肌红蛋白缺失的免疫组化研究

作者应用免疫组比技术（ＡＢＣ）对青壮年淬死综合征及对照组病例的心肌肌红：蛋白缺失情况进行了研究，并经扫描显微镜光度计测量分析，结果发现青壮年猝死综合征组心肌肉肌红蛋白均有不同程度的缺失，多数病例呈多发、散在、节段性分布，而对照组无明显缺失。认为这种多发、散在、节段性的肌红蛋白缺失与其仅有不同程度的心肌缺血而未出现大片心肌梗死有关，而这种不同程度的心肌缺血很可能为冠状动脉痉挛所致。     

The Role of Postmortem Cardiac Markers in the Diagnosis of Acute Myocardial Infarction*

Abstract: Sudden cardiac deaths because of acute myocardial infarction (MI) constitute a significant percentage of the caseload for death investigators, coroners, and forensic pathologists. Clinicians use cardiac markers, highly sensitive and specific for myocardial damage, to screen living patients for acute MI; however, to this point, the utility of these markers in the autopsy setting has not been fully established. The current study included 10 decedents, five who died of acute MI, and five subjects who died of noncardiac disease. Samples of pericardial fluid and blood from multiple sites were tested for creatine kinase, creatinine kinase MB, and troponin‐I. Three main conclusions were drawn: the levels of cardiac markers from all patients are significantly higher than the reference range for living patients, there are significant differences in cardiac marker levels between samples from different anatomic locations, and only three cardiac marker/anatomic site combinations were significantly different between the control and study groups.     

急性心肌梗死心传导系统的免疫组化实验观察

观察急性心肌梗死时心传导系统的形态学改变。取急性心肌梗死死亡者的心传导系统标本6例,运用抗纤维连接蛋白抗体、肌红蛋白抗体、血管内皮生长因子抗体进行免疫组化染色。结果发现,纤维连接蛋白染色有3例呈现强阳性,2例出现阳性,1例出现弱阳性;血管内皮生长因子染色均呈弱阳性;肌红蛋白染色呈脱失改变。提示纤维连接蛋白检测量敏感性强,稳定性好,易于观察,可作为在心肌梗死时了解心传导系统受损害的指标之一。     

Giant cell myocarditis with cardiac tamponade: a rare combination

Giant cell myocarditis (GCM) is a rare but fatal disease of idiopathic origin. It results in focal necrosis of myocardium. This is a case report of middle aged Malaysian Indian female who died due to cardiac tamponade due to rupture myocardium and tear in the root of aorta. On naked eye examination, it simply resembled as recent as well as old fibrotic areas of myocardial infarction. She was clinically diagnosed as a case of obstructive cardiomyopathy with atrioventricular block, and was on pace maker. There was subendocardial fibrosis and left ventricular transmural infarction in the left ventricle. On histopathology, this was diagnosed as GCM, there were widespread areas of inflammatory cellular infiltration within the myocardium with multinucleated giant cells and granulomas interspersed with lymphocytes. Microscopic field showed up to 10 multinucleated giant cells. In this case, there were focal areas at multiple locations and caused uneven thickness in the left ventricle wall. Idiopathic GCM is very rare and causation of hemopericardium is the unique feature of this case. In this case the direct link of GCM with aortitis and rupture of left ventricle wall resulting in hemopericardium is shown. This case is documented through macroscopic as well as microscopic photographs in H&E, Ziel-Nelson, and GMS staining.