Lundy P M, Gverzdys S, Frew R
Can J Physiol Pharmacol. 1985 Apr;63(4):298-303. doi: 10.1139/y85-054.
Ketamine (1.1 X 10(-5) to 3.7 X 10(-4) M) potentiated catecholamine responses of rat anococcygeus muscle and rabbit aorta in vitro. In the anococcygeus, potentiation was abolished by cocaine (2.9 X 10(-5) M) pretreatment or by chemical sympathectomy using 6-hydroxydopamine (6-OHDA), but was unaffected by pretreatment with the extraneuronal uptake inhibitor cortisol (8.3 X 10(-5) M), or the catechol-O-methyltransferase inhibitor tropolone (2.4 X 10(-4) M). The action of ketamine mimicked the potentiating effect of cocaine on tyramine responses. In contrast, the potentiation by ketamine in rabbit aorta was unaffected by cocaine or 6-OHDA but was abolished by cortisol or tropolone; and ketamine potentiated tyramine responses, whereas cocaine inhibited them. Thus the mechanism of action by which ketamine produces potentiation of catecholamines in these two tissues is completely different. These results suggest that ketamine has the unusual ability to block neuronal and extraneuronal uptake and that the predominating mechanism will depend on the type of tissue examined and the morphology of its adrenergic innervation.
氯胺酮（1.1×10⁻⁵至3.7×10⁻⁴M）在体外增强大鼠肛门尾骨肌和兔主动脉的儿茶酚胺反应。在肛门尾骨肌中，可卡因（2.9×10⁻⁵M）预处理或使用6-羟基多巴胺（6-OHDA）进行化学交感神经切除术可消除增强作用，但不受神经元外摄取抑制剂皮质醇（8.3×10⁻⁵M）或儿茶酚-O-甲基转移酶抑制剂托酚酮（2.4×10⁻⁴M）预处理的影响。氯胺酮的作用模拟了可卡因对酪胺反应的增强作用。相比之下，氯胺酮对兔主动脉的增强作用不受可卡因或6-OHDA的影响，但被皮质醇或托酚酮消除；并且氯胺酮增强酪胺反应，而可卡因抑制它们。因此，氯胺酮在这两种组织中产生儿茶酚胺增强作用的作用机制完全不同。这些结果表明，氯胺酮具有阻断神经元和神经元外摄取的非凡能力，并且主要机制将取决于所检查的组织类型及其肾上腺素能神经支配的形态。
