Horn E P, Standl T, Sessler D I, von Knobelsdorff G, Büchs C, Schulte am Esch J
Department of Anesthesiology, University Hospital Eppendorf, Hamburg, Germany.
Anesthesiology. 1998 Jan;88(1):108-13. doi: 10.1097/00000542-199801000-00018.
Postanesthetic shivering develops in as many as one half of patients recovering from isoflurane anesthesia. Cholinergic stimulation of the hypothalamic-pituitary-adrenal axis and adrenal medulla by physostigmine enhances secretion of arginine vasopressin, epinephrine, and norepinephrine. Because the hypothalamus is the dominant thermoregulatory controller in mammals, and these neurotransmitters may be involved in body temperature control, physostigmine administration may influence the incidence of shivering. Accordingly, the authors tested the hypothesis that physostigmine administration inhibits postanesthetic shivering. Its efficacy was compared with that of saline (negative control) and meperidine and clonidine (positive controls).
Sixty patients having surgery of the ear or nose were tested. General anesthesia was induced with 2 mg/kg propofol, 0.1 mg/kg vecuronium, and 1.5 microg/kg fentanyl and maintained with isoflurane (1.5 +/- 0.4%) in 70% nitrous oxide. At the end of surgery, the patients were randomly assigned to receive an intravenous bolus of 0.04 mg/kg physostigmine, isotonic saline, 0.5 mg/kg meperidine, or 1.5 microg/kg clonidine. Heart rate, mean arterial blood pressure, oxygen saturation, visual analog pain score, temperature, and postanesthetic shivering were measured during recovery.
Postanesthetic shivering occurred in 6 of 15 (40%) patients given saline. In contrast, postanesthetic shivering was significantly reduced in physostigmine-treated patients (1 of 15, or 7%) and was absent in patients given clonidine or meperidine.
Physostigmine inhibited shivering as well as did two established treatments, meperidine and clonidine. These data suggest that cholinergic systems contribute to the genesis and control of postanesthetic shivering.
多达一半接受异氟烷麻醉后恢复的患者会出现麻醉后寒战。毒扁豆碱对下丘脑 - 垂体 - 肾上腺轴和肾上腺髓质的胆碱能刺激可增强精氨酸加压素、肾上腺素和去甲肾上腺素的分泌。由于下丘脑是哺乳动物主要的体温调节控制器，且这些神经递质可能参与体温控制，给予毒扁豆碱可能会影响寒战的发生率。因此，作者检验了给予毒扁豆碱可抑制麻醉后寒战这一假设。将其疗效与生理盐水（阴性对照）以及哌替啶和可乐定（阳性对照）进行比较。
对60例接受耳部或鼻部手术的患者进行测试。采用2mg/kg丙泊酚、0.1mg/kg维库溴铵和1.5μg/kg芬太尼诱导全身麻醉，并用异氟烷（1.5±0.4%）加70%氧化亚氮维持麻醉。手术结束时，将患者随机分为四组，分别静脉推注0.04mg/kg毒扁豆碱、等渗盐水、0.5mg/kg哌替啶或1.5μg/kg可乐定。在恢复过程中测量心率、平均动脉血压、血氧饱和度、视觉模拟疼痛评分、体温以及麻醉后寒战情况。
给予生理盐水的15例患者中有6例（40%）出现麻醉后寒战。相比之下，接受毒扁豆碱治疗的患者麻醉后寒战明显减少（15例中有1例，即7%），而接受可乐定或哌替啶治疗的患者未出现寒战。
毒扁豆碱抑制寒战的效果与两种已确立的治疗药物哌替啶和可乐定相当。这些数据表明胆碱能系统参与了麻醉后寒战的发生和控制。
