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迅速发展的可卡因诱导的外周门静脉肝损伤。

Rapidly developing cocaine-induced peripheral portal liver damage.

作者信息

Charles S J, Powell C J

机构信息

DH Department of Toxicology, St Bartholomews Hospital Medical College, London, UK.

出版信息

Toxicol Lett. 1992 Dec;64-65 Spec No:729-37. doi: 10.1016/0378-4274(92)90254-h.

Abstract

Cocaine administration to phenobarbitone treated DBA/2Ha mice caused scattered peripheral portal cell necrosis within 2 h. At 3 h, when this initial lesion had become more widespread, and plasma membrane integrity had been compromised, 15-fold elevations in plasma levels of liver enzymes were observed. Biochemical analysis of liver microsomes showed no changes in the levels of total cytochrome P-450 during the development of hepatic damage, and there was no correlation between microsomal malondialdehyde (MDA), an indicator of lipid peroxidation, and liver damage. These results indicate that as liver damage occurs only 2 h after cocaine administration, prompt action is warranted when cocaine overdose is suspected.

摘要

给用苯巴比妥治疗的DBA/2Ha小鼠注射可卡因,2小时内会导致散在的外周门管区细胞坏死。3小时时,最初的损伤变得更广泛,质膜完整性受到损害,观察到肝酶血浆水平升高了15倍。肝微粒体的生化分析显示,在肝损伤发展过程中,总细胞色素P-450水平没有变化,脂质过氧化指标微粒体丙二醛(MDA)与肝损伤之间也没有相关性。这些结果表明,由于可卡因给药后仅2小时就会发生肝损伤,因此当怀疑可卡因过量时,应立即采取措施。

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