Sessler D I, Olofsson C I, Rubinstein E H
Department of Anesthesia, University of California, San Francisco 94143-0648.
Anesthesiology. 1988 Sep;69(3):357-64. doi: 10.1097/00000542-198809000-00012.
Narcotics and nitrous oxide (N2O) inhibit thermoregulatory responses in animals. The extent to which N2O/fentanyl anesthesia lowers the thermoregulatory threshold in humans was tested by measuring peripheral cutaneous vasoconstriction using skin-surface temperature gradients (forearm temperature-fingertip temperature) and the laser Doppler perfusion index. Fifteen unpremedicated patients were anesthetized with N2O (70%) and fentanyl (10 micrograms/kg iv bolus followed by 4 micrograms.kg-1.h-1 infusion) during elective, donor nephrectomy. Patients were randomly assigned to undergo additional warming (humidified respiratory gases, warmed intravenous fluids, and a heating blanket over the legs; n = 5) or standard temperature management (no special warming measures; n = 10). Significant vasoconstriction was prospectively defined as a skin-surface temperature gradient between forearm surface and finger-tip surface greater than or equal to 4 degrees C, and the thermoregulatory threshold was defined as the esophageal temperature at which such vasoconstriction occurred. Vasoconstriction did not occur in the patients who received additional warming and thus remained nearly normothermic [average minimum esophageal temperature = 35.8 +/- 0.4 degrees C (SD)] but did in six hypothermic patients at a mean esophageal temperature of 34.2 +/- 0.5 degrees C. Four hypothermic patients developed a passive thermal steady state without becoming sufficiently cold to trigger vasoconstriction. Thus, active thermoregulation occurs during N2O/fentanyl anesthesia but does not occur until core temperatures are approximately 2.5 degrees C lower than normal. The thermoregulatory threshold during N2O/fentanyl anesthesia is similar to that previously determined during halothane (34.4 +/- 0.2 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)
麻醉药和一氧化二氮（N₂O）会抑制动物的体温调节反应。通过使用皮肤表面温度梯度（前臂温度 - 指尖温度）和激光多普勒灌注指数测量外周皮肤血管收缩，来测试N₂O/芬太尼麻醉降低人体体温调节阈值的程度。15名未使用术前药的患者在择期供体肾切除术中接受N₂O（70%）和芬太尼（静脉推注10微克/千克，随后以4微克·千克⁻¹·小时⁻¹输注）麻醉。患者被随机分配接受额外保暖措施（湿化呼吸气体、温热静脉输液以及腿部覆盖加热毯；n = 5）或标准体温管理（无特殊保暖措施；n = 10）。显著血管收缩被前瞻性定义为前臂表面与指尖表面之间的皮肤表面温度梯度大于或等于4摄氏度，体温调节阈值被定义为发生这种血管收缩时的食管温度。接受额外保暖的患者未发生血管收缩，因此体温几乎保持正常[平均最低食管温度 = 35.8 ± 0.4摄氏度（标准差）]，但6名体温过低的患者在平均食管温度为34.2 ± 0.5摄氏度时发生了血管收缩。4名体温过低的患者达到了被动热稳态，但未冷到足以触发血管收缩。因此，在N₂O/芬太尼麻醉期间会发生主动体温调节，但直到核心温度比正常低约2.5摄氏度时才会发生。N₂O/芬太尼麻醉期间的体温调节阈值与先前在氟烷麻醉期间确定的阈值相似（34.4 ± 0.2摄氏度）。（摘要截断于250字）
