Inomata S, Nishikawa T, Kihara S, Akiyoshi Y
Department of Anaesthesia, Iwaki Kyoritsu General Hospital, Fukushima, Japan.
Can J Anaesth. 1995 Feb;42(2):119-25. doi: 10.1007/BF03028263.
Clonidine, an alpha 2-adrenergic agonist, augments the pressor response to intravenous ephedrine. If this effect is partly due to clonidine-induced potentiation of alpha 1-adrenoceptor-mediated vasoconstriction, it is also assumed that clonidine would enhance the pressor effect of phenylephrine as an alpha 1-adrenergic agonist. The authors studied haemodynamic responses to intravenous phenylephrine in 80 patients who received either preanaesthetic medication with clonidine approximately 5 micrograms.kg-1 po (clonidine group, n = 40), or no medication (control group, n = 40). Each group was further divided into either awake subjects (n = 20) or subjects anaesthetized with enflurane and nitrous oxide in oxygen (n = 20). Haemodynamic measurements were made at one-minute intervals for ten minutes after phenylephrine 2 micrograms.kg-1 iv was injected as a bolus. The magnitudes of maximal mean blood pressure increases in the clonidine group (26 +/- 7% (mean +/- SD) for awake and 32 +/- 15% for anaesthetized subjects) were greater (P < 0.05) than in the control group (13 +/- 7% for awake and 18 +/- 7% for anaesthetized subjects). However, there was no difference in the pressor effect of phenylephrine between awake and anaesthetized patients in both groups. Oral clonidine preanaesthetic medication, 5 micrograms.kg-1, augments the pressor responses to phenylephrine 2 micrograms.kg-1 iv in awake and anaesthetized patients. These results suggest that the enhancement of the pressor responses to phenylephrine following oral clonidine may be due to clonidine-induced potentiation of alpha 1-adrenoceptor-mediated vasoconstriction. This implies that restoration of blood pressure can be achieved effectively by phenylephrine in hypotensive patients with clonidine premedication.
可乐定是一种α2肾上腺素能激动剂,可增强静脉注射麻黄碱后的升压反应。如果这种效应部分归因于可乐定诱导的α1肾上腺素能受体介导的血管收缩增强,那么也可以认为可乐定作为一种α1肾上腺素能激动剂会增强去氧肾上腺素的升压作用。作者研究了80例患者静脉注射去氧肾上腺素后的血流动力学反应,这些患者中40例在麻醉前口服约5微克/千克的可乐定(可乐定组),另外40例未用药(对照组)。每组又进一步分为清醒受试者(n = 20)或用安氟醚和笑气-氧气麻醉的受试者(n = 20)。在静脉推注2微克/千克去氧肾上腺素后,每隔1分钟进行10分钟的血流动力学测量。可乐定组最大平均血压升高幅度(清醒受试者为26±7%(平均值±标准差),麻醉受试者为32±15%)大于对照组(清醒受试者为13±7%,麻醉受试者为18±7%)(P < 0.05)。然而,两组中清醒和麻醉患者之间去氧肾上腺素的升压作用没有差异。麻醉前口服5微克/千克的可乐定可增强清醒和麻醉患者对2微克/千克静脉注射去氧肾上腺素的升压反应。这些结果表明,口服可乐定后去氧肾上腺素升压反应增强可能是由于可乐定诱导的α1肾上腺素能受体介导的血管收缩增强。这意味着在可乐定预处理的低血压患者中,去氧肾上腺素可有效恢复血压。