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。     

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。     

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。     

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     

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。     

定量检测NSE和S-100推断脑挫伤时间的动物实验

观察实验性大鼠脑挫伤后NSE、S－100的时间性变化规律,为法医学推断脑挫伤形成时间提供新的手段。采用改进的Feeney氏落体打击致Wistar大鼠脑挫伤模型,进行免疫组织化学SP法染色,并利用图像分析仪对免疫组化染色阳性细胞灰度和面积进行测量,SAS统计软件分析,结果显示：NSE阳性神经元灰度与面积在伤后1h至2d呈下降趋势,至伤后12h阳性细胞灰度、面积降到最小值（P＜0．01）;S－100阳性细胞面积和灰度伤后呈上升趋势,至伤后4dS－100阳性细胞灰度、面积达到最大值,与对照组及其它实验组比较均有显著性差异（P＜0．01）,伤后5d仍保持较高水平;NSE、S－100免疫组织化学染色阳性细胞的数量、灰度、面积改变有时间规律。推断2d内脑挫伤可用NSE作为主要指标,推断2～5d的脑挫伤则以S－100改变为主。     

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     

早期心肌缺血心肌肌红蛋白变化的免疫组织化学研究

本实验应用免疫组织化学方法对12只犬急性冠脉阻断60及90分钟后心肌肌红蛋白变化情况进行了研究.结果表明心肌缺血60分钟已有明显的肌红蛋白脱失,比相应H、E 染色切片更易辨认缺血灶,在H、E 染色改变不明显的区域,免疫组织化学染色已显示出肌红蛋白的缺失.冠脉阻断90分钟时,缺血区肌红蛋白缺失更加清晰,因此该方法可用于诊断早期心肌缺血,结果可靠.     

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.     

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.     

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。     

大鼠早期心肌缺血纤维蛋白原与肌红蛋白的免疫组织化学对比性研究

按Selye法结扎Wistar大鼠冠状动脉左前降支，复制早期心肌缺血（EMI）模型。根据心肌缺血不同时间（15min、30min、1h、2h、3h）分5个实验组，另设1个对照组；每组取心尖部及其邻近的心肌组织制成石蜡切片，进行HE、链霉系合素生物素过氧化物酶（SAB）染色。结果表明：早期心肌缺血30min组，缺血区心肌即出现肌红蛋白（Mb）缺失和纤维蛋白原（Fg）染色增强。随着缺血时间延长，Mb缺失或Fg染色增强范围扩大，程度加重，从心内膜下向外层心肌发展呈“波浪式推进现象”，二者在心肌缺血过程中的变化规律相同，灵敏度相似，但Fg易受血液污染而致其可靠性较Mb差。在注意血液污染的前提下，SABC－Fg技术为诊断EMI提供了新的途径。     

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。     

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。     

早期心肌缺血心脏型脂肪酸结合蛋白的免疫组织化学观察

目的探讨心脏型脂肪酸结合蛋白(H-FABP)对早期心肌缺血诊断的灵敏性。方法应用免疫组织化学技术对正常心脏、心肌梗死及其它怀疑有心肌缺血的心肌细胞内H-FABP和肌红蛋白(Mb)的变化进行研究。结果正常对照组均无明显的缺失,心肌梗死组均出现明显的缺失,9例可疑心肌缺血病例中有3例出现H-FABP明显的缺失,3例出现可疑缺失,有4例出现Mb明显的缺失,2例出现可疑缺失,说明H-FABP可用于诊断早期心肌缺血。结论H-FABP用于诊断早期心肌缺血具有较好的灵敏性。