大鼠早期心肌缺血心肌肌钙蛋白T脱失的组化研究

目的研究早期心肌缺血大鼠模型上心肌肌钙蛋白T的脱失情况。方法应用免疫组化LSAB法显色观察。结果缺血15分钟,大鼠心肌肌钙蛋白T即有明显脱失,随缺血时间的延长,脱失面积呈扩大趋势。计算机图像分析显示缺血大鼠心肌肌钙蛋白T的脱失面积与正常大鼠心肌之间存在显著性差异。结论心肌肌钙蛋白T是诊断早期心肌缺血的较为敏感的指标之一。     

实验性早期心肌梗死的肌红蛋白免疫组织化学研究

结扎大鼠冠状动脉前降支,制造早期(5分钟到24小时)心肌梗死模型.用抗肌红蛋白抗体免疫组织化学技术(PAP法)观察大鼠心肌梗死区肌红蛋白脱失(缺染)情况,结果表明:冠状血管结扎后30分钟,梗死区少数心肌出现轻度不完全性缺染;结扎2-6小时,梗死区心肌缺染范围扩大呈带状、条状、片状;结扎lO-24小时,梗死区心肌缺染范围达全层,大部分属完全性缺染,与非梗死区分界清晰.     

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     

结蛋白诊断早期心肌梗死的特异性研究

目的　探讨结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他非梗死性的直接或间接心肌损害的心肌结蛋白染色的变化。结果梗死心肌均可见不同程度的结蛋白缺染 ,其他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 ,也有不同程度的结蛋白缺染。结论　应用结蛋白免疫组织化学方法诊断早期心肌梗死需慎重     

结蛋白诊断早期心肌梗死的特异性研究

目的 探讨结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他非梗死性的直接或间接心肌损害的心肌结蛋白染色的变化。结果 梗死心肌均可见不同程度的结蛋白缺染,其他非梗死性的直接或间接心肌损害的心肿,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,也有不同程度的结蛋白缺染。 结论 应用结蛋白免疫组织化学方法诊断早期心肌梗死需慎重。     

心肌缺血猝死心肌中高迁移率族蛋白B-1的表达研究

目的探讨高迁移率族蛋白B-1(High Mobility Group Box protein 1,HMGB1)在心肌缺血猝死后诊断中的法医学价值。方法收集不同案例心肌蜡块分为疑似早期心肌缺血猝死组(早期梗死组)20例、心肌梗死猝死组(心肌梗死组)15例、冠心病非心源性猝死组(对照组1)10例和正常心肌组(对照组2)10例,应用免疫组织化学二步法染色,观察心肌胞核和胞浆中HMGB1表达,用ImagePro Plus 6.0软件计算HMGB1表达的平均光密度,用SPSS 13.0对表达进行数据统计分析。结果 HMGB1在四组心肌细胞胞核中表达均呈阳性;早期梗死组和心肌梗死组胞浆均呈阳性表达,对照组1和对照组2胞浆呈阴性。各组平均光密度分别为0.3031±0.0557、0.3195±0.0523、0.0252±0.0030、0.0207±0.0029,早期梗死组和心肌梗死组的阳性反应与两个对照组相比存在显著差异(P﹤0.01)。结论 HMGB1可作为早期心肌缺血猝死的一个辅助诊断指标。     

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     

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、出血性休在克、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梗死慎重。     

急性心肌缺血猝死心肌中血红素加氧酶-1的表达

目的观察血红素加氧酶-1（HO-1）在急性心肌缺血猝死心肌细胞胞浆中的表达情况。方法应用免疫组织化学技术（SP法）,对27例可疑早期心肌缺血猝死（早期梗死组）、10例心肌梗死猝死（心肌梗死组）、11例冠心病非心性猝死（对照组1）以及10例正常心肌（对照组2）中HO-1的表达进行观察分析。结果早期梗死组与心肌梗死组在心肌细胞胞浆中HO-1均呈强阳性表达,对照组1和对照组2心肌细胞胞浆中HO-1弱阳性表达或无表达。早期梗死组和心肌梗死组与对照组1和对照组2之间心肌细胞内HO-1表达的差异有显著性意义（P（0.01）;镜下各组心肌细胞胞浆内HO-1表达的阳性面积率及平均光密度差别明显。结论 HO-1可以作为急性心肌缺血所致心性猝死的一个诊断指标。     

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。     

Cardiac troponin T (cTn T) and the postmortem diagnosis of sudden death

PURPOSE: To evaluate the effectiveness of the increase of postmortem cardiac troponin T (cTn T) in acute disease-related deaths. METHODS: Peripheral venous blood was sampled from 39 autopsies performed. Thirty nonhemolyzed specimens were considered in the final analysis (n = 30).Only the calculation of the cTn T was performed using the Roche Diagnostics Elecsys 2010 Immunoassay System. The high limit and the cutoff are 25 ng/mL.Deaths were divided into 2 groups, according to sudden cardiac deaths (group 1, n = 15) and non-cardiac-related deaths without resuscitation (group 2, n = 15). RESULTS: All the cases with visual myocardial infarction had elevated concentrations of cTn T. The difference of the postmortem cTn T concentrations between resuscitated and nonresuscitated is nonsignificant.In the non-cardiac-related deaths, the elevated concentrations of cTn T were only noted in all cases of electrocution. CONCLUSION: In clinical practice, several biochemical markers are used for the diagnosis of myocardial infarction. Because of its extreme specificity for myocardial damage, cTn T and cardiac troponin I (cTn I) are frequently used. The results of these assays could then be used to facilitate selection for cases that may be released following histologic examinations.     

Evaluation of cardiac troponin I immunoreaction in autopsy hearts: a possible marker of early myocardial infarction

Postmortem diagnosis of early myocardial infarctions is an ever recurrent problem in pathology. In the present study we determined the troponin I expression in 46 autopsy hearts using an immunohistochemical technique. Troponin I has, as a specific cardiac muscle protein, become a widespread used marker in testing patients with acute chest pain. The hearts were divided into three groups based on the macroscopical findings: definite signs of infarction, possible signs of infarction and no signs of infarction. All 14 cases of definite myocardial infarction showed a well-defined area with loss of troponin I. Twenty-three of 24 cases of possible myocardial infarction also showed a well-defined area with loss of troponin I. None of the eight non-cardiac death controls showed loss of troponin I expression. The results suggest troponin I expression as a sensitive test in diagnosis of early myocardial infarction.     

Serum concentrations of cardiac troponin T in sudden death

Ischemic heart disease is the most common cause of sudden death of natural causes in most western countries. By autopsy, there may be no gross or histologic evidence of acute myocardial damage unless the patient survived for several hours following the event. Cardiac troponin in serum has become the recommended biochemical marker for myocardial injury in the clinical setting. We performed a prospective study on 102 autopsied subjects at the Central Hospital of Rogaland, Stavanger, Norway. Femoral blood was sampled for subsequent analysis of cardiac troponin T (cTnT). In the subjects with morphologic evidence of recent myocardial injury (n = 34), the mean serum cTnT level was 1.95 microg/L compared with 0.16 microg/L in the subjects with a noncardiac cause of death (n = 35) and 0.61 microg/L in the group with probable sudden cardiac death without morphologic signs of acute myocardial injury (n = 33). The observed differences in mean serum cTnT levels between the groups were statistically significant (P < 0.0001). These data suggest that elevated postmortem serum concentration of cTnT reflects ongoing myocardial damage and may support a diagnosis of cardiac-related death in cases associated with sparse or inconclusive morphologic findings postmortem.     

Heart fatty acid binding protein as a marker for postmortem detection of early myocardial damage

Depletion of heart fatty acid binding protein (H-FABP) from cardiomyocytes with varying post-ischemia intervals was studied in acute myocardial infarction (AMI) model of rat, and 22 human autopsy cases were studied with streptavidin-peroxidase conjugated method (S-P). It was observed that as early as 15 min after ischemia, the depletion of H-FABP could be detected in model rats. With the ischemic time prolonged, the depletion of H-FABP was more and more evident. In all human cases with myocardial infarction, absent H-FABP staining could be found in infarcted area. And in some suspected early myocardial infarction cases, depletion of H-FABP staining could be demonstrated in areas that showed normal hematoxylin-eosin (HE) staining. The blood samples from model rats before ligation, at varying post-ischemia intervals and various postmortem time were measured for plasma concentration of H-FABP with enzyme-linked immuno-sorbent assay (ELISA) method. At 15 min after myocardial ischemia, the concentration of H-FABP was 4 times higher (546.0+/-85.3 microg/l) than that of the baseline level (103.7+/-94.1 microg/l). With the continuation of ischemic time, the concentration of H-FABP increased and peaked at 4 h (1953.5+/-405.3 microg/l), then decreased. The plasma concentration of H-FABP decreased slightly with postmortem time, but was still significant higher at any postmortem intervals than that of baseline level within 48 h after death. The results suggest that H-FABP staining can detect very early ischemic damages in human myocardium and the elevated plasma concentration of H-FABP in rat was an indicator of AMI, which was not affected by autolysis.     

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。     

缺血修饰白蛋白在急性缺血性心脏病中的法医学应用

目的探讨心包液中缺血修饰白蛋白(ischemia modified albumin,IMA)水平在心脏性猝死诊断中的应用价值及法医学意义。方法应用白蛋白-钴离子结合法检测急性缺血性心脏病组(36例)、急性心肌梗死组(6例)、心肌病组(4例)、对照组(15例)死者的心包液中IMA水平,比较各组之间IMA水平的差异。通过ROC曲线获得最佳IMA水平的截断值以及区分急性缺血性心脏病和对照组的敏感度和特异度。结果急性缺血性心脏病组心包液中IMA水平高于对照组(P0.05);而与急性心肌梗死组、心肌病组心包液中IMA水平比较,差异均无统计学意义(P0.05)。应用ROC曲线分析得出识别急性心肌缺血的IMA的截断值为40.65 U/m L,其诊断急性心肌缺血的敏感度为60.0%,特异度为80.5%。结论心包液中IMA有望作为诊断急性心肌缺血的参考指标,为心脏性猝死的法医学诊断提供客观依据。     

Detection of apoptosis in ischemic heart. Usefulness in the diagnosis of early myocardial injury

Myocardial samples of hearts with histologic findings of acute myocardial infarction (group A), sudden coronary deaths without histologic changes (group B), and chronic ischemic heart disease (group C) were analyzed to investigate the appearance of apoptosis in acute and chronic ischemic cardiac disorders. This analysis involved the morphologic detection of DNA strand breaks in myocyte nuclei by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay and the biochemical determination of DNA laddering in the myocardium using archival formalin-fixed, paraffin-embedded tissue sections of human myocardium. The authors demonstrated that apoptosis of myocardial cells could occur after ischemic myocardial cell injury. In all documented cases of acute myocardial infarction (group A), the infarcted area included extensive presence of both apoptosis and necrosis. In the tissue bordering on and away from the obviously infarcted areas, positive nuclei were intermingled with nonstained normal myocytes. The number of positive nuclei decreased with the distance from the infarction foci. In group B, myocardial samples showed focal or diffuse nuclear positivity of varying degrees for apoptosis, confirming the presence of myocardial ischemic cell death, whereas the histologic diagnosis remained inconclusive. This finding suggests that apoptosis could be used as a marker for acute ischemic injury. In group C, stained nuclei were dispersed with intermingled normal cardiomyocytes.     

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.     

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。