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活体和死后创伤性心肌损伤后的免疫组化改变

Immunohistochemical alterations after intravital and post-mortem traumatic myocardial damage.

作者信息

Ortmann C, Pfeiffer H, Brinkmann B

机构信息

Institut für Rechtsmedizin, Westfälische Wilhelms-Universität, Münster, Germany.

出版信息

Int J Legal Med. 2001 Aug;115(1):23-8. doi: 10.1007/s004140100216.

DOI:10.1007/s004140100216
PMID:11599765
Abstract

Two series of experiments have been carried out on heart tissue for the occurrence of post-mortem and intravital myocardial damage. The first series was carried out on 18 porcine hearts collected immediately after the pigs were killed in a slaughterhouse. The hearts were subjected to stab wounds post-mortem, varying between 5 min and 140 min after death. The second series investigated were human hearts with intravital damage, i.e. 4 stab wounds, 1 gunshot, 13 contusions and ruptures. The time the trauma occurred before death varied between 0 and 30 min. The investigation comprised the four myocyte structural proteins myoglobin, FABP, troponin C, desmin and the three plasma proteins fibrinogen, fibronectin and C5b-9. Both series exhibited a variety of direct traumatic changes with a much broader zone in vital damage compared to post-mortem damage. In vital damage the zone of direct damage is in continuity with a further zone of indirect damage which is a three dimensional network. The signs of damage are contraction bands, depletion of structure antigens, contraction-associated accumulation of structure proteins, accumulation of plasma proteins on the cell surfaces and in the interstitium. In vital damages there is in addition an intrasarcolemmal accumulation of plasma proteins. The pattern of all damage is much broader and much more variegated in vital damage, thus vital damage can be clearly differentiated from post-mortem damage. bin, heart-type fatty acid binding protein (FABP), troponin, desmin, fibrinogen and fibronectin (Amberg 1995; Brinkmann et al. 1993; Glatz et al. 1994; Kleine et al. 1993; Leadbetter et al. 1989; Ortmann et al. 2000a, 2000b; Osuna et al. 1998; Thomsen and Held 1994, 1995). The aim of the present study was to elaborate reaction patterns of these marker proteins in mechanical heart trauma induced ante- and post-mortem and to explore their value for wound age determination in forensic casework.

摘要

为研究死后和生前心肌损伤的发生情况,对心脏组织进行了两个系列的实验。第一个系列实验是对18个在屠宰场宰杀后立即采集的猪心脏进行的。这些心脏在死后受到刺伤,死亡时间在5分钟至140分钟之间不等。第二个系列实验研究的是生前受损的人类心脏,即4处刺伤、1处枪伤、13处挫伤和破裂伤。创伤发生至死亡的时间在0至30分钟之间。研究包括四种心肌细胞结构蛋白,即肌红蛋白、心脏型脂肪酸结合蛋白(FABP)、肌钙蛋白C、结蛋白,以及三种血浆蛋白,即纤维蛋白原、纤连蛋白和C5b - 9。两个系列实验均呈现出各种直接创伤性变化,与死后损伤相比,生前损伤的损伤区域要广泛得多。在生前损伤中,直接损伤区域与一个进一步的间接损伤区域相连,间接损伤区域是一个三维网络。损伤迹象包括收缩带、结构抗原耗竭、与收缩相关的结构蛋白积聚、血浆蛋白在细胞表面和间质中的积聚。在生前损伤中,血浆蛋白还会在肌膜内积聚。所有损伤模式在生前损伤中要广泛得多且更加多样,因此生前损伤可与死后损伤明显区分开来。肌红蛋白、心脏型脂肪酸结合蛋白(FABP)、肌钙蛋白、结蛋白、纤维蛋白原和纤连蛋白(安贝格,1995年;布林克曼等人,1993年;格拉茨等人,1994年;克莱内等人,1993年;利德贝特等人,1989年;奥尔特曼等人,2000年a,2000年b;奥苏纳等人,1998年;汤姆森和赫尔德,1994年,1995年)。本研究的目的是阐述这些标记蛋白在生前和死后机械性心脏创伤中的反应模式,并探讨它们在法医案件工作中用于确定伤口时间的价值。

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