心肌病猝死者心肌连接蛋白43的免疫组化染色观察

目的探讨心肌病猝死者心肌连接蛋白43(Cx43)染色变化及其与猝死的关系。方法运用免疫组化和图像分析技术,分2组(A和B组)检测20例心肌病猝死者心室肌的Cx43染色情况;并与14例非心肌病猝死者(C组)的检测结果对照。结果扩张型心肌病(DCM)猝死组(A组,11例)心肌Cx43染色明显减弱,阳性着色斑点大小不等、深浅不一、分布不均,有的呈散在颗粒状;其它类型的心肌病猝死组(B组,9例)亦见类似变化;非心肌病猝死的对照组(C组,14例)未见明显变化。定量检测并经统计分析发现,Cx43蛋白染色阳性的面积,A组与B组和C组的差异有非常显著性意义(P<0.01),B组与C组的差异无显著性意义(P>0.05);而平均光密度各组之间的差异无显著性意义(P>0.05)。结论心肌病猝死者心肌Cx43免疫组化染色明显减弱,尤以扩张型心肌病明显;心肌病猝死者心肌Cx43变化可能与其猝死有一定关系。     

儿茶酚胺致心肌损伤的实验病理研究

大鼠尾静脉滴去甲肾上腺素（20μg／kg／min）后，分别于即刻、7天、30～90天杀死取材，用病理组织学、肌红蛋白免疫组化染色及透射电镜观察心肌损伤。结果：早期可见心肌多灶性坏死、肌红蛋白缺染、肌原纤维断裂溶解，似冠状动脉无阻塞性心肌梗死；中后期可见心肌灶性萎缩及疤痕形成、成纤维细胞增生活跃、新生胶元原纤维伸入坏死心肌内，类似早期心肌病图象。     

心肌收缩带坏死在心源性猝死中的病理学特征

目的探讨心肌收缩带坏死在心源性猝死中的病理学特征及意义。方法采用常规HE和PTAH染色方法制片,对心肌收缩带坏死的分布部位、病理学特征等进行观察,并按照坏死程度分级进行分析。结果心肌收缩带坏死在各猝死案例中的分布部位、病理学特征及坏死程度相似,其分布部位与心肌受损的部位有关,左心室乳头肌最易出现,其次为左心室前壁。应激性心肌病导致的猝死中心肌收缩带坏死程度较轻,以1级为多见,其他心肌病以2级为多见。结论心肌收缩带坏死可作为心肌急性缺血的诊断依据,并对死因的判断具有重要意义。     

显示和判定心肌早期病变的染色方法研究

作者用探讨的变色酸2R亮绿法和其他10余种染色方法,对心血管病猝死的尸检心肌和经心电、Mb、CPK、LDH、SOD诊断有急性心肌损伤的多种大量动物实验材料观察结果,证明心肌早期病变有染色性质异常,对显示和判定心肌早期病变有实用价值。提出并讨论了心肌早期病变及其显示、判定方法。     

儿茶酚胺致心肌损伤的病理实验研究

大鼠尾静脉滴注去甲肾上腺素后不同时期(即刻、7、30、90、150天)分别处死取材,用病理组织学、肌红蛋白免疫组化染色及透射电镜观察心肌损伤。结果:急性期心肌呈多灶性坏死,肌红蛋白缺染,肌原纤维溶解断裂,类似人冠状动脉无阻塞性心肌梗塞;急性期后心肌继续灶性溶解、萎缩,成纤维细胞增生活跃,新生胶原纤维伸入心肌坏死灶及其周围间隙,使病灶疤痕化及内膜增厚,类似人早期心肌病病理图象。     

致心律不齐性右室心肌病的研究进展

致心律不齐性右室心肌病是以右室心肌被纤维脂肪取代为特征的一种原因不明的心肌病。通常表现为局限性右室病变。亦可弥漫性进展，侵犯左室。最终导致左心功能不全。近年来，致心律不齐性右室心肌病导致心源性猝死已越来越引起人们的注意。在法医实际工作中。相关研究报道较少。本文综述了致心律不齐性右室心肌病的发病病因、发病机理、病理变化、临床特点和鉴别诊断等方面的研究进展。     

病毒性心肌炎和扩张性心肌病中Dystrophin蛋白的表达

目的探讨病毒性心肌炎和扩张性心肌病的发病机制及相互关系,从而提高心性猝死法医学鉴定的可靠性和准确性。方法对17例对照(包括正常心脏、冠心病、高血压性心脏病等),25例病毒性心肌炎和28例扩张性心肌病的心肌组织进行改良的病理学dystrophin免疫组织化学研究。结果dystrophin蛋白在对照组,病毒性心肌炎组和扩张性心肌病组中阳性表达率分别为100%,88%,57%,三组表达差异有显著性(P<0.05),且在病毒性心肌炎和扩张性心肌病组间表达有显著差异(P<0.05),经Spearman等级相关分析呈显著负相关(r=-0.526)。结论病毒性心肌炎和扩张性心肌病心肌中细胞骨架蛋白均有破坏,且随着由病毒性心肌炎进展为扩张性心肌病,dystrophin蛋白表达逐渐降低,说明在病毒性心肌炎和扩张性心肌病的发病机制中可能与dystrophin的被破坏有关,病毒感染并破坏心肌细胞骨架蛋白并最终导致心肌细胞坏死,心功能受损,从而使病毒性心肌炎进展为扩张性心肌病。     

Fn免疫组化染色在人病毒性心肌炎死后诊断中的应用

目的研究纤维连接蛋白(Fn)免疫组化染色对轻度病毒性心肌炎的病理学诊断价值。方法运用兔抗人Fn多克隆抗体对人类心肌炎心肌标本进行Fn-LSAB免疫组化研究。结果发现心肌炎心肌组织内Fn大量沉积,部分心肌细胞内Fn阳性。结论Fn-LSAB染色可显示轻度病毒性心肌炎的心肌损害,Fn沉积是心肌组织存在炎症性病理变化的可靠标志之一。     

实验性病毒性心肌炎纤维连接蛋白的免疫组化研究

探索轻度病毒性心肌炎的法医病理学诊断方法。以适量coxsackieB3病毒感染Balb/c小鼠 ,造成小鼠轻度病毒性心肌炎 ,对病鼠的心肌进行纤维连接蛋白的LSAB免疫组化染色。结果发现 ,心肌炎鼠心肌组织内Fn大量沉积 ,部分心肌细胞内Fn阳性。Fn -LSAB染色可显示病毒性心肌炎轻度的心肌损害 ,Fn沉积是心肌组织存在炎症性病理变化的可靠标志之一。     

对抗肌动蛋白单克隆抗体诊断早期心肌梗死的评价

为了探讨抗肌动蛋白单克隆抗体（ＨＨＦ３５）在早期心肌梗死死后诊断的特异性，作者用免疫组织化学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ＨＨＦ３５染色的变化。结果：梗死心肌均可见不同程度的ＨＨＦ３５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、机械性窒息等，也有不同程度的ＨＨＦ３５缺染。因此用ＨＨＦ３５免疫组织化学方法诊断早期心肌梗死需慎重     

Diagnostic role of acute microscopic changes in myocardium

Forensic medical diagnosis of death from coronary heart disease, acute ethanol poisoning, alcoholic cardiomyopathy, closed cardiac injuries, mechanical injuries incompatible with life which may be directly caused by acute cardiac failure, requires identification and evaluation of diagnostic complexes of acute myocardial changes. The diagnostic significance of such complexes of myocardial changes is characterized for the first time. A method for evaluation of such changes, addressed to expert histologists, is presented.     

Alcoholic cardiomyopathy versus chronic myocarditis--immunohistological investigations with LCA, CD3, CD68 and tenascin

Dilated cardiomyopathy (DCM) is a disorder of unknown aetiology characterized by the left ventricular cavity enlargement and wall thinning associated with reduced left ventricular wall motion. DCM in chronic alcoholics is supposed to be caused by alcohol induced myocardial damage (alcoholic cardiomyopathy). Nevertheless, cardiotropic viruses, such as enteroviruses have long been suspected as causative agents for at least some forms of DCM. In the present study, 13 cases of DCM in chronic alcoholics were investigated with qualification and quantification of infiltrating leucocytes using immunohistological antibodies against leucocyte common antigen (LCA), T-lymphocytes (CD3) and macrophages (CD68). In addition, the expression of tenascin, playing a role in the initiation of fibrotic changes, was examined. All antigens were known to be possibly enhanced in cases of chronic myocarditis. Using these immunohistological techniques, 2 out of 13 cases had evidence for chronic inflammatory myocardial alterations in the sense of lymphocytic infiltrates (>2.0 CD3 T-lymphocytes/visual field at 400 x (HPF); >7 CD3 T-lymphocytes per mm(2)). These cases were diagnosed as having inflammatory cardiomyopathy. The other cases without myocardial inflammation were diagnosed as idiopathic/alcoholic DCM.     

Microscopic myocardial changes and their significance for forensic medical diagnosis

Morphological myocardial changes essential for diagnosis in forensic medical medicine are listed as well as alterations in the vessels of the myocardium, cardiac muscular fibers and cardiomyocytes important for diagnosis of death of ischemic heart disease, acute alcohol poisoning, alcohol cardiomyopathy, closed cardiac lesions. Changes induced by reflex impacts on the heart and postmortem alterations are also shown.     

Cardiac β1-adrenoceptor expression in two stress-induced cardiomyopathy-related deaths

Stress-induced cardiomyopathy (SICM) is characterized by transient systolic dysfunction of the apical and/or midventricular myocardial segments in the absence of obstructive coronary artery disease and is unique in that it can manifest itself after acute emotional stress. Excessive amounts of catecholamines released from sympathetic nerve endings as well as from the adrenal medulla under stressful conditions are considered to produce intracellular Ca(2+) overload and cardiac dysfunction through the β(1)-adrenoceptor signal transduction pathway. We describe the clinical and pathomorphological findings in two stress-induced cardiomyopathy fatal cases. Levels of catecholamines and their metabolites in urine samples were assessed too. Morphological patterns seen in SICM result from the complex interplay between sympathetic innervations, β-receptor density and function and catecholamine sensitivity.     

Immunocytochemical diagnosis of early myocardial ischaemic/hypoxic damage

The sensitive and reliable dinitrophenyl (DNP) hapten sandwich staining (DHSS) procedure (B. Jasani et al., Virchows Arch (Pathol. Anat.), 406 (1985) 441-448) was used to study the distribution of immunoperoxidase staining seen with antibodies to seven protein markers in post-mortem heart tissue. This was obtained from 12 cases with macroscopic myocardial infarction and 17 cases without myocardial infarction (10 with and 7 without significant coronary artery atherosclerosis). The immunostaining patterns were compared with the appearances seen in adjacent sections stained by the routine haematoxylin and eosin (H & E) and phosphotungstic acid haematoxylin (PTAH) methods and a method previously recommended for the detection of early myocardial infarction, the haematoxylin basic fuchsin picric acid (HBFP) stain. Loss of immunostaining with an antibody to myoglobin was found to be a reliable and more objective marker of both early and established myocardial infarction compared with the histological stains. Antibodies to myosin, caeruloplasmin, C-reactive protein and pre-albumin gave similar but less reliable results, whilst those to complement factor C3b and alpha-1 anti-trypsin gave the least reliable results for early myocardial ischaemic/hypoxic damage. The immunocytochemical results are considered sufficiently encouraging to extend the work to a large number of sudden death cases in order to establish a new, more reliable approach to the detection of histologically latent ischaemic/hypoxic damage in the myocardium.     

早期心肌缺血猝死心肌NF-κB p65的表达研究

目的探讨核因子NF-κBp65（NF-κB p65）在心肌早期缺血猝死后诊断中的法医学价值。方法将收集的案例心肌蜡块分为3组：正常对照组（3例）、早期心肌缺血组（14例）、心肌梗死组（8例）,采用免疫组织化学技术（SP法）,观察猝死心肌内NF-κBp65的表达情况,并对其结果进行半定量分析。结果早期心肌缺血组和心肌梗死组的心肌细胞胞浆内及细胞核内均出现NF-κBp65的表达,且早期心肌缺血组与心肌梗死组表达强度无差异。结论NF-κBp65可以作为早期心肌缺血猝死的一个辅助诊断指标。     

大鼠早期心肌缺血CX43免疫组化研究

目的探讨早期心肌缺血的法医病理学诊断依据。方法通过建立大鼠心肌缺血模型,用免疫组化染色方法检测大鼠心肌缺血15、30、60、120、180min以及正常对照组心肌CX43的表达情况。结果在各组早期心肌缺血区内,见CX43阳性着色的分布与正常组相比,表现为部位的不同及数量上的差异。结论CX43的免疫组化染色对诊断早期心肌缺血有一定的价值,但尚需进一步研究证实。