Ozaki M, Sessler D I, Suzuki H, Ozaki K, Tsunoda C, Atarashi K
Department of Anesthesia, Tokyo Women's Medical College, Japan.
Anesth Analg. 1995 Jun;80(6):1212-6. doi: 10.1097/00000539-199506000-00025.
The core temperature triggering thermoregulatory arteriovenous shunt constriction is designated the threshold for vasoconstriction. High thresholds are generally desirable because vasoconstriction helps prevent further core hypothermia by decreasing cutaneous heat loss and constraining metabolic heat to the core thermal compartment. Previous studies suggest that nitrous oxide (N2O) may inhibit thermoregulatory vasoconstriction less than comparable doses of volatile anesthetics. To confirm this impression, we tested the hypothesis that 0.5 minimum alveolar anesthetic concentration (MAC) N2O combined with 0.5 MAC sevoflurane or isoflurane would reduce the vasoconstriction threshold less than 1.0 MAC sevoflurane or isoflurane. With institutional review board approval, we studied 40 patients, aged 20-60 yr, undergoing open abdominal surgery. No premedication was given. Ten patients each were anesthetized with: 1) N2O (50%) and 0.5 MAC sevoflurane (1%); 2) sevoflurane alone (2%); 3) N2O (60%) and 0.5 MAC isoflurane (0.6%); and, 4) isoflurane alone (1.2%). A forearm minus fingertip, skin temperature gradient > or = 0 degree C was considered significant vasoconstriction; the esophageal temperature triggering vasoconstriction identified the threshold. Morphometric characteristics were comparable in each group. The threshold for vasoconstriction was 35.8 +/- 0.3 degrees C in the patients given 50% N2O combined with 0.5 MAC sevoflurane, which was significantly greater than that in those given 1.0 MAC sevoflurane: 35.1 +/- 0.4 degrees C. Similarly, the threshold for vasoconstriction was 35.9 +/- 0.3 degrees C in the patients given 60% N2O combined with 0.5 MAC isoflurane, which was significantly greater than that in those given 1.0 MAC isoflurane: 35.0 +/- 0.5 degrees C. We thus conclude that N2O impairs thermoregulation less than sevoflurane or isoflurane.
触发体温调节性动静脉分流收缩的核心温度被定义为血管收缩阈值。通常希望有较高的阈值，因为血管收缩通过减少皮肤热量散失并将代谢热限制在核心热区，有助于防止核心体温进一步降低。先前的研究表明，与同等剂量的挥发性麻醉药相比，氧化亚氮（N₂O）对体温调节性血管收缩的抑制作用可能较小。为了证实这一观点，我们检验了以下假设：0.5最低肺泡有效浓度（MAC）的N₂O与0.5 MAC的七氟烷或异氟烷联合使用时，相比1.0 MAC的七氟烷或异氟烷，对血管收缩阈值的降低作用更小。经机构审查委员会批准，我们研究了40例年龄在20至60岁之间接受开腹手术的患者。未给予术前用药。每组10例患者分别接受以下麻醉：1）N₂O（50%）和0.5 MAC七氟烷（1%）；2）单独使用七氟烷（2%）；3）N₂O（60%）和0.5 MAC异氟烷（0.6%）；4）单独使用异氟烷（1.2%）。前臂至指尖的皮肤温度梯度≥0℃被视为显著血管收缩；触发血管收缩的食管温度确定阈值。每组的形态学特征具有可比性。接受50% N₂O与0.5 MAC七氟烷联合麻醉的患者，其血管收缩阈值为35.8±0.3℃，显著高于接受1.0 MAC七氟烷麻醉患者的阈值：35.1±0.4℃。同样，接受60% N₂O与0.5 MAC异氟烷联合麻醉的患者，其血管收缩阈值为35.9±0.3℃，显著高于接受1.0 MAC异氟烷麻醉患者的阈值：35.0±0.5℃。因此，我们得出结论，与七氟烷或异氟烷相比，N₂O对体温调节的损害较小。
