Jackson D M
Arzneimittelforschung. 1975 May;25(5):776-80.
Beta-phenylethylamine on injection into mice (100 mg/kg i.p.) produces a marked hyperthermia which is followed by a prolonged hypothermia. The hyperthermic response was studied in this report. The hyperthermic response was inhibited by p-chlorophenylalanine, methysergide, cyproheptadine, alpha-methyl-tyrosine, propranolol, practolol, phenoxybenzamine, phentolamine, haloperidol, pimozide, protriptyline and desipramine. Lysergic acid diethylamide potentiated the response, while p-chloroamphetamine was without effect. While FLA-63 potentiated the response, disulfiram and reserpine were ineffective in preventing the hyperthermia. Nicotinic acid and prostaglandin E1 did not prevent PE induced hyperthermia. It was concluded from these results that PE induced hyperthermia in mice is blocked by agents that reduce the effective concentration of either DA or 5-HT in the central nervous system (by either synthesis inhibitors or receptor blockers). The involvement with catecholaminergic neurons at least was postulated to be a result of PE induced release of DA from DA neurons.
将β-苯乙胺注射到小鼠体内(腹腔注射100毫克/千克)会产生明显的体温过高,随后是长时间的体温过低。本报告对体温过高反应进行了研究。对氯苯丙氨酸、麦角新碱、赛庚啶、α-甲基酪氨酸、普萘洛尔、普拉洛尔、酚苄明、酚妥拉明、氟哌啶醇、匹莫齐特、普罗替林和地昔帕明可抑制体温过高反应。麦角酸二乙酰胺可增强该反应,而对氯苯丙胺则无作用。虽然FLA - 63可增强该反应,但双硫仑和利血平在预防体温过高方面无效。烟酸和前列腺素E1不能预防苯乙胺诱导的体温过高。从这些结果可以得出结论,苯乙胺诱导的小鼠体温过高被降低中枢神经系统中多巴胺(DA)或5 - 羟色胺(5 - HT)有效浓度的药物所阻断(通过合成抑制剂或受体阻滞剂)。至少据推测,儿茶酚胺能神经元的参与是苯乙胺诱导多巴胺能神经元释放多巴胺的结果。