Chan S H
Exp Neurol. 1984 May;84(2):338-46. doi: 10.1016/0014-4886(84)90230-9.
In cats anesthetized with alpha-chloralose and urethane, intravertebral administration of clonidine (4 and 10 micrograms/kg) dose-dependently suppressed the jaw-opening reflex, arterial blood pressure, and heart rate. For a given dose, there was a differential degree of inhibition in the order of analgesia much greater than hypotension greater than bradycardia. Naloxone injections (0.4 and 1.0 mg/kg, i.vert.) essentially failed to antagonize these effects, suggesting the lack of involvement of the opiate receptors or endogenous opioids in these processes. Furthermore, pain suppression by clonidine appeared to be independent of the vasodepression and cardioinhibition it promoted. It is possible that neural mechanisms responsible for clonidine-induced antinociception, hypotension, and bradycardia are likely to have differential sensitivities to the imidazoline compound, regardless of whether they exist in separate central sites or in subpopulations of neurons within common neural substrates.
在用α-氯醛糖和乌拉坦麻醉的猫中,经椎管内给予可乐定(4和10微克/千克)可剂量依赖性地抑制下颌张开反射、动脉血压和心率。对于给定剂量,抑制程度存在差异,顺序为镇痛作用远大于低血压作用大于心动过缓作用。注射纳洛酮(0.4和1.0毫克/千克,椎管内注射)基本未能拮抗这些作用,表明阿片受体或内源性阿片类物质未参与这些过程。此外,可乐定的疼痛抑制作用似乎与其所引发的血管舒张和心脏抑制作用无关。有可能负责可乐定诱导的抗伤害感受、低血压和心动过缓的神经机制对咪唑啉化合物具有不同的敏感性,无论它们是存在于不同的中枢部位还是共同神经基质内的神经元亚群中。