Tarakanov A V
Farmakol Toksikol. 1990 Jul-Aug;53(4):25-8.
The experiments on albino rats showed that clofeline administered in a subanalgesic dose significantly potentiates the analgesic effect of ketamine at the segmental and suprasegmental levels mainly through mu-opiate and partially through beta 2-adrenergic chains. The initiating role in potentiation belongs to the activation of alpha 2-adrenoreceptors. The analgesic effect of ketamine at the segmental and suprasegmental levels is implemented through alpha 2-adrenergic apparatus and at the suprasegmental level is additionally of naloxone-depended character. The clinical trials showed that a preliminary administration of clofeline during postoperative analgesia with ketamine potentiates and prolongs the analgesic action of the latter.
对白化大鼠的实验表明,以亚镇痛剂量给药的氯非宁主要通过μ-阿片受体,部分通过β2-肾上腺素能途径,在节段性和节段以上水平显著增强氯胺酮的镇痛作用。增强作用的起始作用归因于α2-肾上腺素能受体的激活。氯胺酮在节段性和节段以上水平的镇痛作用是通过α2-肾上腺素能机制实现的,而在节段以上水平还具有纳洛酮依赖性特征。临床试验表明,在术后使用氯胺酮镇痛期间预先给予氯非宁可增强并延长后者的镇痛作用。