Yamakage M, Tsujiguchi N, Hattori J, Kamada Y, Namiki A
Department of Anesthesiology, Sapporo Medical University School of Medicine, Japan.
Anesthesiology. 2000 Jul;93(1):179-88. doi: 10.1097/00000542-200007000-00029.
Because exposure to low temperature can modify the effect of volatile anesthetics on airway smooth muscle contraction, this study was conducted to investigate low-temperature modifications of the inhibitory effects of isoflurane and sevoflurane on canine tracheal smooth muscle tone by simultaneously measuring the muscle tension and intracellular concentration of Ca2+ ([Ca2+]i) and by measuring voltage-dependent Ca2+ channel activity.
[Ca2+]i was monitored by the 500-nm light emission ratio of preloaded fura-2, a Ca2+ indicator. Isometric tension was measured simultaneously. Whole cell patch clamp recording techniques were used to observe voltage-dependent Ca2+ channel activity in dispersed muscle cells. Isoflurane (0-3.0%) or sevoflurane (0-3%) was introduced to a bath solution at various temperatures (37, 34, or 31 degrees C).
Low temperature (34 or 31 degrees C) reduced high-K+-induced (72.7 mm) muscle contraction and increased [Ca2+]i, but it enhanced carbachol-induced (1 microm) muscle contraction with a decrease in [Ca2+]i. The volatile anesthetics tested showed significant inhibition of both high-K+-induced and carbachol-induced airway smooth muscle contraction, with a concomitant decrease in [Ca2+]i. The inhibition of the carbachol-induced muscle contraction by volatile anesthetics was abolished partially by exposure to low temperature. Volatile anesthetics and low-temperature exposure significantly inhibited voltage-dependent Ca2+ channel activity of the smooth muscle.
Exposure of airway smooth muscle to low temperature leads to an increase in agonist-induced muscle contractility, with a decrease in [Ca2+]i. The inhibition of voltage-dependent Ca2+ channel activity by exposure to low temperature and by volatile anesthetics cam be attributed, at least in part, to the decrease in [Ca2+]i.
由于低温暴露可改变挥发性麻醉药对气道平滑肌收缩的作用,本研究通过同时测量肌肉张力和细胞内钙离子浓度([Ca2+]i)以及测量电压依赖性钙离子通道活性,来研究低温对异氟烷和七氟烷抑制犬气管平滑肌张力作用的影响。
[Ca2+]i通过预先加载的钙离子指示剂fura-2的500纳米发光比率进行监测。同时测量等长张力。采用全细胞膜片钳记录技术观察分散的肌肉细胞中电压依赖性钙离子通道活性。在不同温度(37、34或31摄氏度)下,将异氟烷(0-3.0%)或七氟烷(0-3%)加入浴液中。
低温(34或31摄氏度)可降低高钾(72.7毫摩尔)诱导的肌肉收缩,并增加[Ca2+]i,但可增强卡巴胆碱(1微摩尔)诱导的肌肉收缩,同时[Ca2+]i降低。所测试的挥发性麻醉药对高钾诱导和卡巴胆碱诱导的气道平滑肌收缩均有显著抑制作用,同时[Ca2+]i降低。挥发性麻醉药对卡巴胆碱诱导的肌肉收缩的抑制作用在低温暴露后部分被消除。挥发性麻醉药和低温暴露显著抑制了平滑肌的电压依赖性钙离子通道活性。
气道平滑肌暴露于低温会导致激动剂诱导的肌肉收缩性增加,同时[Ca2+]i降低。低温暴露和挥发性麻醉药对电压依赖性钙离子通道活性的抑制作用至少部分可归因于[Ca2+]i的降低。