Kozlov S N, Iasnetsov V S
Farmakol Toksikol. 1977 May-Jun;40(3):281-3.
The influence of some neuroleptic, adreno, sympatho- and cholinolytic substances on the development of experimental brain edema induced with nicotine was studied in tests conducted on rats. It was ascertained that marked antiedemic properties display drugs blocking the alpha-adrenoreceptors (phentolamine, dopegit), the neuroleptic chlorpromazine and central M-cholinolytics (benactizine). Weak action exert central H-cholinolytics (difacil trasentin) and the neuroleptic galoperidol. Sympatho- and beta-adrenolytics (guanethidine, alpha-methyltyrosine, obsidan), and also the neuroleptic triphthazine fail to prevent the development of an experimental brain edema. It is presumed that a brain edema induced with nicotine comes as a result of the catecholamines liberation and is also due to stimulation of alpha-adrenoreactive systems.
在对大鼠进行的试验中,研究了某些抗精神病药、肾上腺素能药、交感神经药和抗胆碱药对尼古丁诱发的实验性脑水肿发展的影响。已确定,阻断α-肾上腺素能受体的药物(酚妥拉明、多匹吉特)、抗精神病药氯丙嗪和中枢性M-胆碱能阻断剂(贝那替秦)具有显著的抗水肿特性。中枢性H-胆碱能阻断剂(双苯丙胺、曲美苄胺)和抗精神病药加洛哌丁醇作用较弱。交感神经阻断剂和β-肾上腺素能阻断剂(胍乙啶、α-甲基酪氨酸、澳西丹)以及抗精神病药三氟拉嗪不能预防实验性脑水肿的发展。据推测,尼古丁诱发的脑水肿是儿茶酚胺释放的结果,也是由于α-肾上腺素反应系统受到刺激所致。