可乐定对麻醉状态下的人体产生剂量依赖性的压力反射介导的体温调节反应损害,该反应针对呼气末正压。
Clonidine produces a dose-dependent impairment of baroreflex-mediated thermoregulatory responses to positive end-expiratory pressure in anaesthetized humans.
作者信息
Mizobe T, Nakajima Y, Sunaguchi M, Ueno H, Sessler D I
机构信息
Department of Anesthesiology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
出版信息
Br J Anaesth. 2005 Apr;94(4):536-41. doi: 10.1093/bja/aei086. Epub 2005 Feb 11.
BACKGROUND
Perioperative hypothermia is common and results from anaesthesia-induced inhibition of thermoregulatory control. Hypothermia is blunted by baroreceptor unloading caused by positive end-expiratory pressure (PEEP), and is mediated by an increase in the vasoconstriction threshold. Premedication with clonidine impairs normal thermoregulatory control. We therefore determined the effect of clonidine on PEEP-induced hypothermia protection.
METHODS
Core temperature was evaluated in patients undergoing combined general and epidural anaesthesia for lower abdominal surgery. They were assigned to an end-expiratory pressure of zero (ZEEP) or 10 cm H(2)O PEEP. The PEEP group was divided into three blinded subgroups that received placebo (Cl-0), clonidine 150 microg (Cl-150) and clonidine 300 microg (Cl-300) respectively. Placebo or clonidine was given orally 30 min before surgery. We evaluated core temperature and thermoregulatory vasoconstriction. We also determined plasma epinephrine, norepinephrine, angiotensin II concentrations and plasma renin activity.
RESULTS
Core temperature after 180 min of anaesthesia was 35.1 (0.4) degrees C in the ZEEP group. PEEP significantly increased final core temperature to 35.8 (0.5) degrees C (Cl-0 group). Clonidine produced a linear, dose-dependent impairment of PEEP-induced hypothermia protection: final core temperatures were 35.4 (0.3) degrees C in the Cl-150 group and 35.0 (0.6) degrees C in the Cl-300 group. Similarly, clonidine produced a linear and dose-dependent reduction in vasoconstriction threshold: Cl-0, 36.4 (0.3) degrees C; Cl-150, 35.8 (0.3) degrees C; Cl-300, 35.4 (0.6) degrees C. Plasma norepinephrine, angiotensin II concentrations and renin activity were consistent with the thermoregulatory responses.
CONCLUSION
Baroreceptor unloading by PEEP normally moderates perioperative hypothermia. However, clonidine premedication produces a linear, dose-dependent reduction in this benefit.
背景
围手术期体温过低很常见,是由麻醉诱导的体温调节控制抑制所致。呼气末正压(PEEP)引起的压力感受器卸载可减轻体温过低,其通过血管收缩阈值的升高介导。可乐定术前用药会损害正常的体温调节控制。因此,我们确定了可乐定对PEEP诱导的体温过低保护作用的影响。
方法
对接受下腹部手术的全身麻醉联合硬膜外麻醉患者的核心体温进行评估。他们被分配到呼气末压力为零(ZEEP)或10 cm H₂O PEEP组。PEEP组分为三个盲法亚组,分别接受安慰剂(Cl-0)、150 μg可乐定(Cl-150)和300 μg可乐定(Cl-300)。术前30分钟口服安慰剂或可乐定。我们评估了核心体温和体温调节性血管收缩。我们还测定了血浆肾上腺素、去甲肾上腺素、血管紧张素II浓度和血浆肾素活性。
结果
ZEEP组麻醉180分钟后的核心体温为35.1(0.4)℃。PEEP显著将最终核心体温提高到35.8(0.5)℃(Cl-0组)。可乐定对PEEP诱导的体温过低保护作用产生线性、剂量依赖性损害:Cl-150组的最终核心体温为35.4(0.3)℃,Cl-300组为35.0(0.6)℃。同样,可乐定使血管收缩阈值呈线性和剂量依赖性降低:Cl-0组为36.4(0.3)℃;Cl-150组为35.8(0.3)℃;Cl-300组为35.4(0.6)℃。血浆去甲肾上腺素、血管紧张素II浓度和肾素活性与体温调节反应一致。
结论
PEEP引起的压力感受器卸载通常可减轻围手术期体温过低。然而,可乐定术前用药会使这种益处呈线性、剂量依赖性降低。