Taittonen M T, Kirvelä O A, Aantaa R, Kanto J H
Department of Anesthesiology, Turku University Hospital, Finland.
Anesth Analg. 1998 Jul;87(1):161-7. doi: 10.1097/00000539-199807000-00034.
The use of ketamine as a sole anesthetic induces marked central sympathetic stimulation, causing increased heart rate, blood pressure (BP), and oxygen consumption (VO2). Both alpha 2-agonists and benzodiazepines have been used to attenuate these potentially harmful ketamine-induced responses. This double-blind, randomized, placebo-controlled study was designed to compare the perioperative metabolic, hemodynamic, and sympathoadrenal responses to IM clonidine (2 micrograms/kg) and midazolam (70 micrograms/kg) premedication during ketamine anesthesia. VO2 was measured continuously using indirect calorimetry in 30 ASA physical status I patients. The patients received ketamine, mivacurium, and fentanyl for the induction of anesthesia. Anesthesia was maintained using a ketamine infusion and fentanyl boluses i.v. Preoperatively, both VO2 and BP decreased significantly after the administration clonidine and midazolam compared with placebo (P < 0.01). Intraoperatively, VO2 was higher in the midazolam group than in the placebo and clonidine groups (P < 0.05). Postoperatively, there were no significant differences in BP and VO2, although they stayed at lower level in the clonidine group during the whole postoperative period. Clonidine decreased pre- and postoperative plasma catecholamine concentrations (P < 0.05). Our results indicate that a midazolam-ketamine combination may induce potentially harmful metabolic stimulation, whereas the sympatholytic effects of clonidine on ketamine-anesthetized patients may be beneficial, as perioperative VO2 was decreased.
Ketamine causes sympathetic stimulation with an ensuing increase in oxygen consumption. Anticipating that clonidine might attenuate this response, we measured oxygen consumption in patients undergoing surgery during ketamine anesthesia. Patients treated with a clonidine-ketamine combination had lower intra- and postoperative oxygen consumption than those treated with a midazolam-ketamine combination.
单独使用氯胺酮作为麻醉剂会引起明显的中枢交感神经刺激,导致心率、血压(BP)和氧耗量(VO2)增加。α2激动剂和苯二氮䓬类药物都已被用于减弱这些氯胺酮诱导的潜在有害反应。这项双盲、随机、安慰剂对照研究旨在比较氯胺酮麻醉期间,术前使用肌内注射可乐定(2微克/千克)和咪达唑仑(70微克/千克)进行预处理对围手术期代谢、血流动力学和交感肾上腺系统的反应。使用间接测热法连续测量30例美国麻醉医师协会(ASA)身体状况I级患者的VO2。患者接受氯胺酮、米库氯铵和芬太尼诱导麻醉。使用氯胺酮静脉输注和芬太尼静脉推注维持麻醉。术前,与安慰剂相比,给予可乐定和咪达唑仑后VO2和BP均显著下降(P<0.01)。术中,咪达唑仑组的VO2高于安慰剂组和可乐定组(P<0.05)。术后,BP和VO2无显著差异,尽管可乐定组在整个术后期间保持在较低水平。可乐定降低了术前和术后血浆儿茶酚胺浓度(P<0.05)。我们的结果表明,咪达唑仑 - 氯胺酮组合可能会引起潜在有害的代谢刺激,而可乐定对氯胺酮麻醉患者的交感神经阻滞作用可能是有益的,因为围手术期VO2降低。
氯胺酮引起交感神经刺激,随之氧耗量增加。预期可乐定可能减弱这种反应,我们测量了氯胺酮麻醉期间手术患者的氧耗量。与接受咪达唑仑 - 氯胺酮组合治疗的患者相比,接受可乐定 - 氯胺酮组合治疗的患者术中和术后的氧耗量更低。