Paalzow G H, Paalzow L K
J Pharmacol Exp Ther. 1982 Dec;223(3):795-800.
The antinociceptive effect of clonidine on a response to painful stimulation mediated by supraspinal structures was recorded after s.c. administration of the drug in doses from 50 up to 2000 micrograms/kg. Both low and high doses of clonidine produced antinociception on the pain threshold studied. A careful analysis of the dose-response curve showed, however, that the net effect recorded involved the sum of responses from at least two functional systems or receptor sites. When the dose-response relationship of clonidine-induced antinociception was studied after alpha-1 receptor blockade by means of phenoxybenzamine, it was found that this effect comprised contributions from different neurotransmitter systems. These results are discussed in terms of the possibility that separate adrenergic receptors mediate clonidine antinociception at different levels in the pain transmission. The determinant of the population of receptors being activated after systemic administration of clonidine is the dose given.
在皮下注射剂量为50至2000微克/千克的可乐定后，记录了可乐定对脊髓上结构介导的疼痛刺激反应的抗伤害感受作用。低剂量和高剂量的可乐定都对所研究的疼痛阈值产生了抗伤害感受作用。然而，对剂量反应曲线的仔细分析表明，所记录的净效应涉及至少两个功能系统或受体位点的反应总和。当通过酚苄明阻断α-1受体后研究可乐定诱导的抗伤害感受的剂量反应关系时，发现这种效应包括不同神经递质系统的贡献。根据不同的肾上腺素能受体在疼痛传递的不同水平介导可乐定抗伤害感受的可能性对这些结果进行了讨论。全身给药后被激活的受体群体的决定因素是所给予的剂量。
