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非人类免疫缺陷病毒感染的吸毒者的神经病理学:慢性静脉吸毒后的缺氧性脑损伤。

Neuropathology in non-human immunodeficiency virus-infected drug addicts: hypoxic brain damage after chronic intravenous drug abuse.

作者信息

Oehmichen M, Meissner C, Reiter A, Birkholz M

机构信息

Institut für Rechtsmedizin, Medizinischen Universität zu Lübeck, Germany.

出版信息

Acta Neuropathol. 1996;91(6):642-6. doi: 10.1007/s004010050478.

Abstract

Neuropathological studies were carried out on 180 human immunodeficiency virus-seronegative intravenous drug addicts. The findings in victims of acute heroin intoxication (n = 116) were congestion (99.1%), capillary engorgement (68.1%), and/or perivascular bleeding (68.1%) - hemodynamic processes attributable to toxic primary respiratory failure. In a high percentage of these cases (88%), cerebral edema was also present. In 18 cases of acute heroin intoxication who survived for periods of hours or days, the sole postmortem finding was ischemic nerve cell damages, resembling that typically seen in systemic hypoxia. Semiquantitative analysis revealed nerve cell loss in the hippocampal formation and/or Purkinje cell layer in 26% of the 162 chronic drug abusers. By contrast, in nearly 80% of these cases, the hippocampus showed enhanced expression of glial fibrillary acid protein by astrocytes and/or a proliferation of microglia, demonstrated by CD68 expression. Since such reactive processes are produced by primary neuronal damages, it can be assumed that chronic intravenous drug abuse results in obviously ischemic nerve cell loss. This could be demonstrated in the hippocampus, but it must also occur throughout the whole brain. The demonstration of ischemic nerve cell damage and neuronal loss or secondary reactive alterations has not been described previously.

摘要

对180名人类免疫缺陷病毒血清阴性的静脉注射吸毒者进行了神经病理学研究。急性海洛因中毒受害者(n = 116)的发现包括充血(99.1%)、毛细血管充血(68.1%)和/或血管周围出血(68.1%)——这些是由中毒性原发性呼吸衰竭引起的血流动力学过程。在这些病例中,很大比例(88%)还存在脑水肿。在18例存活数小时或数天的急性海洛因中毒病例中,唯一的尸检发现是缺血性神经细胞损伤,类似于系统性缺氧时常见的损伤。半定量分析显示,在162名慢性吸毒者中,26%的人海马结构和/或浦肯野细胞层存在神经细胞丢失。相比之下,在这些病例中,近80%的海马显示星形胶质细胞胶质纤维酸性蛋白表达增强和/或小胶质细胞增殖,通过CD68表达得以证明。由于这些反应性过程是由原发性神经元损伤引起的,可以假设慢性静脉注射吸毒会导致明显的缺血性神经细胞丢失。这在海马中可以得到证明,但也必定在整个大脑中发生。缺血性神经细胞损伤以及神经元丢失或继发性反应性改变此前尚未见报道。

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