Weitz J D, Foster S D, Waugaman W R, Katz R L, Bloor B C
Nurse Anesth. 1991 Mar;2(1):19-27.
Dexmedetomidine, an alpha 2-adrenergic agonist, was administered during isoflurane anesthesia to investigate its anesthetic sparing and hemodynamic effects in the canine model. Eleven healthy dogs were anesthetized with isoflurane, intubated, and allowed to breathe spontaneously. The animals were instrumented in order to measure or calculate mean arterial blood pressure (MABP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), cardiac output (CO), and systemic vascular resistance (SVR). Isoflurane minimum alveolar concentration (MAC), baseline hemodynamic measurements, and plasma catecholamine levels were determined. A 20 micrograms/kg bolus of dexmedetomidine was injected intravenously (IV) and MAC and hemodynamic values were redetermined. When isoflurane requirements were 33% of baseline, isoflurane was returned to 90% MAC and the alpha 2-antagonist, atipamezole, was administered. All dogs were treated with 40 micrograms/kg glycopyrrolate throughout the experiment to prevent any bradycardic response. Dexmedetomidine reduced isoflurane MAC by 86%. SVR, MABP, and LVEDP were significantly increased while CO and catechloamine levels were reduced. Atipamezole fully reversed the reduction in anesthetic requirements. MABP and catecholamine levels returned to baseline. SVR and LVEDP increased while CO decreased. The dogs exhibited a profound reduction in anesthetic requirement, reduced catecholamine levels, and changes in hemodynamic parameters with dexmedetomidine administration. The anesthetic sparing effect appears to be mediated by the alpha 2-receptor, since atipamezole reversed the reduction in MAC. Hemodynamic changes may be species or dose related, or due to differences in existing sympathetic tone. The role of dexmedetomidine warrants further study as an adjunct anesthetic agent.
右美托咪定是一种α2肾上腺素能激动剂，在异氟烷麻醉期间给药，以研究其在犬模型中的麻醉协同作用和血流动力学效应。11只健康犬用异氟烷麻醉，插管，并允许自主呼吸。对动物进行仪器监测，以测量或计算平均动脉血压（MABP）、心率（HR）、左心室舒张末期压力（LVEDP）、心输出量（CO）和全身血管阻力（SVR）。测定异氟烷最低肺泡浓度（MAC）、基线血流动力学测量值和血浆儿茶酚胺水平。静脉注射（IV）20微克/千克的右美托咪定推注剂量，然后重新测定MAC和血流动力学值。当异氟烷需求量为基线的33%时，将异氟烷恢复至90%MAC，并给予α2拮抗剂阿替美唑。在整个实验过程中，所有犬均接受40微克/千克的格隆溴铵治疗，以防止任何心动过缓反应。右美托咪定使异氟烷MAC降低了86%。SVR、MABP和LVEDP显著升高，而CO和儿茶酚胺水平降低。阿替美唑完全逆转了麻醉需求的降低。MABP和儿茶酚胺水平恢复至基线。SVR和LVEDP升高，而CO降低。给予右美托咪定后，犬的麻醉需求显著降低，儿茶酚胺水平降低，血流动力学参数发生变化。麻醉协同作用似乎是由α2受体介导的，因为阿替美唑逆转了MAC的降低。血流动力学变化可能与物种或剂量有关，也可能是由于现有交感神经张力的差异。右美托咪定作为辅助麻醉剂的作用值得进一步研究。
