Sessler D I, Olofsson C I, Rubinstein E H, Beebe J J
Department of Anesthesia, University of California, San Francisco 94143-0648.
Anesthesiology. 1988 Jun;68(6):836-42. doi: 10.1097/00000542-198806000-00002.
Although suppression of thermoregulatory mechanisms by anesthetics is generally assumed, the extent to which thermoregulation is active during general anesthesia is not known. The only thermoregulatory responses available to anesthetized, hypothermic patients are vasoconstriction and non-shivering thermogenesis. To test anesthetic effects on thermoregulation, the authors measured skin-surface temperature gradients (forearm temperature--finger-tip temperature) as an index of cutaneous vasoconstriction in unpremedicated patients anesthetized with 1% halothane and paralyzed with vecuronium during elective, donor nephrectomy. Patients were randomly assigned to undergo maximal warming (warm room, humidified respiratory gases, and warm intravenous fluids; n = 5) or standard temperature management (no special warming measures; n = 5). Skin-surface temperature gradients greater than or equal to 4 degrees C were prospectively defined as significant vasoconstriction. Normothermic patients [average minimum esophageal temperature = 36.4 +/- 0.3 degrees C (SD)] did not demonstrate significant vasoconstriction. However, each hypothermic patient displayed significant vasoconstriction at esophageal temperatures ranging from 34.0 to 34.8 degrees C (average temperature = 34.4 +/- 0.2 degrees C). These data indicate that active thermoregulation occurs during halothane anesthesia, but that it does not occur until core temperature is approximately equal to 2.5 degrees C lower than normal. In two additional hypothermic patients, increased skin-temperature gradients correlated with decreased perfusion as measured by a laser Doppler technique. Measuring skin-surface temperature gradients is a simple, non-invasive, and quantitative method of determining the thermoregulatory threshold during anesthesia.
虽然通常认为麻醉药会抑制体温调节机制，但在全身麻醉期间体温调节的活跃程度尚不清楚。麻醉状态下体温过低的患者唯一可用的体温调节反应是血管收缩和非寒战产热。为了测试麻醉对体温调节的影响，作者在择期供体肾切除术中，测量了未用术前药、用1%氟烷麻醉并用维库溴铵麻痹的患者的皮肤表面温度梯度（前臂温度 - 指尖温度），以此作为皮肤血管收缩的指标。患者被随机分配接受最大程度的保暖措施（温暖的房间、加湿的呼吸气体和温暖的静脉输液；n = 5）或标准温度管理（无特殊保暖措施；n = 5）。前瞻性地将皮肤表面温度梯度大于或等于4℃定义为显著血管收缩。体温正常的患者[平均最低食管温度 = 36.4 ± 0.3℃（标准差）]未表现出显著血管收缩。然而，每例体温过低的患者在食管温度为34.0至34.8℃（平均温度 = 34.4 ± 0.2℃）时均表现出显著血管收缩。这些数据表明，在氟烷麻醉期间存在活跃的体温调节，但直到核心温度比正常温度低约2.5℃时才会出现。在另外两名体温过低的患者中，皮肤温度梯度增加与激光多普勒技术测量的灌注减少相关。测量皮肤表面温度梯度是一种简单、非侵入性且定量的方法，可用于确定麻醉期间的体温调节阈值。
