Aki Toshihiko, Unuma Kana
Department of Forensic Medicine, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Histol Histopathol. 2025 Sep;40(9):1339-1346. doi: 10.14670/HH-18-904. Epub 2025 Mar 13.
Cocaine is a psychostimulant abused worldwide. Its pharmacotoxicological properties are derived mainly from its impact on the neurotransmission of sympathomimetic nerves. Cocaine enhances and prolongs the neurotransmission of monoamines, such as dopamine, serotonin, and adrenaline, which are responsible not only for cocaine's euphoric effects, but also its cardiovascular toxicity. In addition to these effects on central as well as peripheral nerves, immunosuppression is also implicated in cocaine toxicity. The thymus and spleen are lymphoid organs that are essential in lymphocyte maturation and erythrocyte homeostasis. Reductions in thymus and spleen size, which are observed under both physiological and pathological conditions, are known as thymic involution and splenic contraction, respectively. These phenomena are also observed in experimental animal models of binge cocaine abuse. In this brief review, we describe the mechanisms of cocaine toxicity, thymic involution, and splenic contraction, followed by discussions about the possible role of the latter two phenomena in cocaine intoxication.
可卡因是一种在全球范围内被滥用的精神兴奋剂。其药物毒理学特性主要源于它对拟交感神经神经传递的影响。可卡因增强并延长单胺类神经递质(如多巴胺、血清素和肾上腺素)的传递,这些单胺不仅导致可卡因的欣快感,还会引发其心血管毒性。除了对中枢和外周神经的这些影响外,免疫抑制也与可卡因毒性有关。胸腺和脾脏是淋巴细胞成熟和红细胞稳态所必需的淋巴器官。在生理和病理条件下观察到的胸腺和脾脏大小减小,分别称为胸腺退化和脾脏收缩。在滥用可卡因的实验动物模型中也观察到了这些现象。在这篇简短的综述中,我们描述了可卡因毒性、胸腺退化和脾脏收缩的机制,随后讨论了后两种现象在可卡因中毒中可能发挥的作用。