Department of Anesthesiology, Nara Medical University, Nara, Japan.
Minerva Anestesiol. 2010 Dec;76(12):1002-9. Epub 2010 Sep 13.
Beta-1-receptor blockade reduces heart rate, cardiac output, and arterial pressure while increasing peripheral vascular resistance. It is possible that beta blockers not only inhibit the core-to-peripheral re-distribution of body heat and cutaneous heat loss due to vasodilation after anesthesia induction but also reduce the convective transfer of heat from the core to peripheral tissues by decreasing cardiac output. The authors investigated whether the co-administration of esmolol or landiolol, ultra-short-acting beta blockers, attenuates the magnitude of initial re-distribution hypothermia after anesthesia induction and tracheal intubation.
Immediately prior to the induction of anesthesia, patients were randomly assigned to receive 0.2 mg kg-1 of landiolol (landiolol group; N=30), 1 mg kg-1 of esmolol (esmolol group; N=30), or 0.1 mL kg-1 of saline (control group; N=30). Heart rate, blood pressure, cardiac output, and tympanic, forearm, and digit temperatures were recorded. Forearm minus fingertip skin-surface temperature gradients (temperature gradient) were calculated.
Tympanic membrane temperatures 15 to 60 min after the induction of anesthesia were significantly higher in the esmolol group than in the control group although the temperature gradient was similar among the three groups. Both esmolol and landiolol inhibited the increase in HR and MAP after the induction of anesthesia and tracheal intubation. The cardiac index in the esmolol group was significantly lower than in the control group. The degree of hemodynamic attenuation after induction by esmolol was larger than that of landiolol.
The co-administration of esmolol, but not landiolol, attenuated the magnitude of initial re-distribution hypothermia after anesthesia induction and tracheal intubation. Esmolol likely prevented initial hypothermia because it attenuated the convective transfer of heat from the core to peripheral tissues by decreasing cardiac output.
β-1 受体阻滞剂可降低心率、心输出量和动脉压，同时增加外周血管阻力。β 受体阻滞剂不仅可能抑制麻醉诱导后血管扩张导致的核心到外周体热再分布和皮肤散热减少，而且可能通过降低心输出量减少核心到外周组织的热对流转移。作者研究了超短效β受体阻滞剂艾司洛尔或拉地洛尔是否能减轻麻醉诱导和气管插管后初始再分布性低体温的程度。
在麻醉诱导前，患者被随机分为三组：静脉给予 0.2mg/kg 拉地洛尔（拉地洛尔组，n=30）、1mg/kg 艾司洛尔（艾司洛尔组，n=30）或 0.1mL/kg 生理盐水（对照组，n=30）。记录心率、血压、心输出量以及鼓膜、前臂和指温。计算前臂与指尖皮肤表面温度梯度（温度梯度）。
麻醉诱导后 15-60min 鼓膜温度在艾司洛尔组明显高于对照组，尽管三组之间温度梯度相似。艾司洛尔和拉地洛尔均抑制麻醉诱导和气管插管后 HR 和 MAP 的增加。艾司洛尔组的心指数明显低于对照组。艾司洛尔诱导后的血液动力学抑制程度大于拉地洛尔。
艾司洛尔而非拉地洛尔的联合应用减轻了麻醉诱导和气管插管后的初始再分布性低体温。艾司洛尔可能通过降低心输出量来预防初始低体温，因为它减少了核心到外周组织的热对流转移。
