Golanov E V, Fufacheva A A, Cherkovich G M, Parin S B
Biull Eksp Biol Med. 1987 Apr;103(4):424-7.
Intravenous naloxone injection (0.1 mg/kg) facilitated blood pressure increase in response to conditioned sound stimulus followed by electrocutaneous shock in conscious chair-restrained baboons (Papio hamadryas). Naloxone at a dose of 1.0 mg/kg had an opposite effect and led to the decrease in blood pressure and heart rate in conditioned fear reflex. Naloxone microinjections (50 microM) into the periventricular hypothalamus led to a significant diminution of blood pressure and heart rate increment in response to electrocutaneous shock; naloxone microinjections into tractus solitarius nuclei suppressed blood pressure and heart rate reactions both to conditioned (sound) and unconditioned (electrocutaneous shock) stimuli. Microinjections of equimolar morphine quantities in these brain regions facilitated such reactions. It is concluded that endogenous opioid system participates in the formation of cardiovascular reactions to emotional stimuli in monkeys, with multiple opioid receptors of periventricular hypothalamus and tractus solitarius nuclei involved in the generation of such reactions.
静脉注射纳洛酮(0.1毫克/千克)可促进清醒的、坐在椅子上受约束的狒狒(阿拉伯狒狒)在条件性声音刺激后紧接着电皮肤休克时血压升高。剂量为1.0毫克/千克的纳洛酮则产生相反的效果,导致条件性恐惧反射中血压和心率下降。向室周下丘脑微量注射纳洛酮(50微摩尔)会显著减弱电皮肤休克引起的血压和心率升高;向孤束核微量注射纳洛酮会抑制对条件性(声音)和非条件性(电皮肤休克)刺激的血压和心率反应。在这些脑区微量注射等摩尔量的吗啡会促进此类反应。得出的结论是,内源性阿片系统参与猴子对情绪刺激的心血管反应的形成,室周下丘脑和孤束核的多种阿片受体参与此类反应的产生。