Zhou Jing, Iwasaki Sohshi, Yamakage Michiaki
From the *Department of Anesthesiology, Shengjing Hospital, China Medical University, Shenyang, China; and †Department of Anesthesiology, Sapporo Medical University, Sapporo, Japan.
Anesth Analg. 2017 Feb;124(2):465-471. doi: 10.1213/ANE.0000000000001754.
Although the bronchodilatory actions of volatile anesthetics, such as halothane, isoflurane, and sevoflurane, have been well documented in previous studies, the properties of desflurane remain controversial. The aim of this study was to investigate the effects of desflurane at different concentrations and durations in an ovalbumin-sensitized guinea pig model of airway hyper-responsiveness.
Ovalbumin-sensitized animals (n = 176) were randomly assigned to 5 groups according to the minimum alveolar concentration (MAC) of desflurane they received: 0.0, 0.5, 1.0, 1.5, and 2.0 MAC. Total lung resistance in vivo, airway smooth muscle tension in vitro, and intracellular cyclic adenosine monophosphate (AMP) levels were measured to evaluate the effects of desflurane.
In 5 sensitized groups, total lung resistance increased from baseline to peak at approximately 8 minutes and then decreased slowly until about 17 minutes with extended administration of desflurane. Desflurane dose-dependently increased total lung resistance with or without incremental doses of acetylcholine and reduced muscle tension with increasing concentrations of carbacholine. Cyclic AMP levels were increased by desflurane: at the 60-minute time point, cyclic AMP concentrations (means ± SD) with 0.5 MAC (1.96 ± 0.40) and 1.0 MAC (2.11 ± 0.50) desflurane were higher than those at the 8-minute time point (1.11 ± 0.23 and 1.32 ± 0.32).
Desflurane exerted time- and dose-dependent effects and could be used at 0.5 and 1.0 MAC concentrations without significant bronchoconstriction in ovalbumin-sensitized guinea pigs. Cyclic AMP-mediated airway smooth muscle relaxation might be one mechanism by which desflurane induces bronchodilation.
尽管之前的研究已充分证明了氟烷、异氟烷和七氟烷等挥发性麻醉剂的支气管扩张作用,但地氟烷的特性仍存在争议。本研究的目的是在卵清蛋白致敏的气道高反应性豚鼠模型中,研究不同浓度和持续时间的地氟烷的作用。
将卵清蛋白致敏的动物(n = 176)根据所接受的地氟烷最低肺泡浓度(MAC)随机分为5组:0.0、0.5、1.0、1.5和2.0 MAC。测量体内总肺阻力、体外气道平滑肌张力和细胞内环磷酸腺苷(AMP)水平,以评估地氟烷的作用。
在5个致敏组中,随着地氟烷持续给药,总肺阻力在约8分钟时从基线升至峰值,然后缓慢下降,直至约17分钟。无论有无递增剂量的乙酰胆碱,地氟烷均剂量依赖性地增加总肺阻力,且随着卡巴胆碱浓度增加降低肌肉张力。地氟烷可提高环磷酸腺苷水平:在60分钟时间点,0.5 MAC(1.96±0.40)和1.0 MAC(2.11±0.50)地氟烷组的环磷酸腺苷浓度高于8分钟时间点(1.11±0.23和1.32±0.32)。
地氟烷具有时间和剂量依赖性作用,在卵清蛋白致敏的豚鼠中,使用0.5和1.0 MAC浓度时不会引起明显的支气管收缩。环磷酸腺苷介导的气道平滑肌舒张可能是地氟烷诱导支气管扩张的一种机制。