Roberts S M, James R C, Harbison R D, Grund V R
Life Sci. 1987 May 25;40(21):2103-10. doi: 10.1016/0024-3205(87)90104-4.
A number of histamine receptor agonists and antagonists were utilized to study the effects of histamine on hepatocellular reduced glutathione (GSH) concentrations and the potential role of histamine as a mediator of morphine-induced hepatic GSH depression. Administration of histamine, the H1-histamine receptor agonist thiazolylethylamine, the H2-histamine receptor agonist impromidine, or the histamine-releasing substance compound 48/80 resulted in no significant change in hepatic GSH concentrations. The H1-histamine receptor antagonist chlorpheniramine and the H2-histamine receptor antagonist ranitidine were also without significant effect on hepatic GSH and did not antagonize morphine-induced GSH depression. These observations indicate that histamine release following morphine administration does not play a significant role in the subsequent depletion of hepatic GSH.
使用了多种组胺受体激动剂和拮抗剂来研究组胺对肝细胞内还原型谷胱甘肽（GSH）浓度的影响，以及组胺作为吗啡诱导的肝脏GSH降低的介质的潜在作用。给予组胺、H1组胺受体激动剂噻唑乙胺、H2组胺受体激动剂英普咪定或组胺释放物质化合物48/80后，肝脏GSH浓度无显著变化。H1组胺受体拮抗剂氯苯那敏和H2组胺受体拮抗剂雷尼替丁对肝脏GSH也无显著影响，且不能拮抗吗啡诱导的GSH降低。这些观察结果表明，吗啡给药后释放的组胺在随后的肝脏GSH耗竭中不起重要作用。
