Gomes C, Svensson T H, Trolin G
J Neural Transm. 1976;39(1-2):33-46. doi: 10.1007/BF01248764.
Morphine caused in the anaesthetized rat reduction in brain noradrenaline (NA) turnover, hypotension and bradycardia, similarly to the antihypertensive, alpha-adrenergic agonist, clonidine. All effects of morphine were antagonized by naloxone, as well as the alpha-receptor antagonist, yohimbine. In contrast, naloxone did not affect the circulatory depression and reduction in brain NA utilization by clonidine which both previously have been found to be antagonized by yohimbine. In contrast to clonidine, morphine even in high doses did not facilitate the flexor reflex activity of acutely spinalized rats. Pretreatment with protriptylin largely attenuated the circulatory depressive effects of morphine, as it has previously been found to block the corresponding effects of clonidine. Thus, the morphine-induced cardiovascular depressive effects are primarily elicited by activation of opiate receptors. However, the inhibition of brain NA neurotransmission by morphine appears critically involved in the mediation of the circulatory depression.
吗啡在麻醉大鼠中引起脑去甲肾上腺素（NA）周转率降低、低血压和心动过缓，这与抗高血压的α-肾上腺素能激动剂可乐定相似。吗啡的所有作用均被纳洛酮以及α-受体拮抗剂育亨宾所拮抗。相比之下，纳洛酮并不影响可乐定引起的循环抑制和脑NA利用减少，而这两者之前已被发现可被育亨宾拮抗。与可乐定不同，即使大剂量吗啡也不会促进急性脊髓损伤大鼠的屈肌反射活动。丙咪嗪预处理在很大程度上减弱了吗啡的循环抑制作用，正如之前发现它可阻断可乐定的相应作用一样。因此，吗啡诱导的心血管抑制作用主要是由阿片受体激活引起的。然而，吗啡对脑NA神经传递的抑制似乎在循环抑制的介导中起关键作用。
