较之异氟醚，七氟醚可最大程度减轻大鼠肺源性急性呼吸窘迫综合征引起的肺损伤
本公众号每天分享一篇最新一期Anesthesia & Analgesia等SCI杂志的摘要翻译，敬请关注并提出宝贵意见
Sevoflurane, Compared With Isoflurane, Minimizes Lung Damage in Pulmonary but Not in Extrapulmonary Acute Respiratory Distress Syndrome in Rats
背景与目的
挥发性麻醉药能调节急性呼吸窘迫综合征（ARDS）中的炎症反应。而它们是否因为ARDS病因的不同而呈现出不同作用，目前尚不十分清楚。我们假设体内、体外实验中，七氟醚和异氟醚在肺源性（p）和非肺源性（exp）ARDS对肺损伤的影响中不存在差异。
方 法
24只Wistar大鼠随机分为七氟醚麻醉组和异氟醚麻醉组（接受麻醉1-2分钟）。动物再随机接受气管内（ARDSp）或腹腔注射（ARDSexp）大肠杆菌脂多糖（LPS）。ARDS诱导24小时后，在1个MAC浓度下进行七氟醚或异氟醚麻醉60分钟。主要观察指标为肺组织白细胞介素(IL)-6 mRNA的表达。次要观察指标包括气体交换功能，肺力学测试，组织学检测，IL-10 mRNA的表达，核因子NF-E2相关因子2 (Nrf2)，表面活化蛋白(SP)-B，血管细胞粘附分子-1，阿米洛利敏感钠通道亚单位α和γ及钠钾ATP泵亚基α1（α1-Na,K-ATPase）β1(β1-Na,K-ATPase)。把其他接受硫喷妥钠麻醉并不行机械通气(NV)的ARDSp和ARDSexp老鼠（n = 6）作为对照组，另外，为研究七氟醚和异氟醚如何作用于肺泡II型上皮细胞，A549人肺上皮细胞接受LPS (20 µg/mL)刺激24小时，暴露在1个MAC浓度七氟醚或异氟醚下60分钟后，对SP-B的表达进行定量。
结 果
对于ARDSp，七氟醚比异氟醚更大程度上降低IL-6的表达(P = .04)。七氟醚静态肺弹性阻力(P = .0049) 及肺泡萎陷程度(P = .033) 较异氟醚低。而Nrf2（P = .036）， SP-B （P = .042），和β1-NA，K-ATP酶（P = .038）在七氟醚均显著高表达。 对于ARDSexp，七氟醚和异氟醚在肺力学、肺泡塌陷或分子参数上无显著差异。在体外，SP-B的表达七氟醚明显比异氟醚高（P = .026）。
结 论
与异氟醚相比，七氟醚对ARDSexp的肺部炎症无影响，但它确实减少ARDSp的肺部炎症。
原始文献摘要
Araújo MN1, Santos CL, Samary CS, Anesth Analg. 2017 Aug;125(2):491-498. doi: 10.1213/ANE.0000000000001927
BACKGROUND:Volatile anesthetics modulate inflammation in acute respiratory distress syndrome (ARDS). However, it is unclear whether they act differently depending on ARDS etiology. We hypothesized that the in vivo and in vitro effects of sevoflurane andisoflurane on lung damage would not differ in pulmonary (p) and extrapulmonary (exp) ARDS.
METHODS:Twenty-four Wistar rats were randomized to undergo general anesthesia (1-2 minutes) with sevoflurane and isoflurane. Animals were then further randomized to receive Escherichia coli lipopolysaccharide (LPS) intratracheally (ARDSp) or intraperitoneally (ARDSexp), and 24 hours after ARDS induction, they were subjected to 60 minutes of sevoflurane or isoflurane anesthesia at 1 minimal alveolar concentration. The primary outcome measure was interleukin (IL)-6 mRNA expression in lung tissue. Secondary outcomes included gas exchange, lung mechanics, histology, and mRNA expression of IL-10, nuclear factor erythroid 2-related factor-2 (Nrf2), surfactant protein (SP)-B, vascular cell adhesion molecule-1, epithelial amiloride-sensitive Na-channel subunits α and γ, and sodium-potassium-adenosine-triphosphatase pump subunits α1 (α1-Na,K-ATPase) and β1 (β1-Na,K-ATPase). Additional ARDSp and ARDSexp animals (n = 6 per group) were anesthetized with sodium thiopental but not mechanically ventilated (NV) to serve as controls. Separately, to identify how sevoflurae and isoflurane act on type II epithelial cells, A549 human lung epithelial cells were stimulated with LPS (20 µg/mL) for 24 hours, and SP-B expression was quantified after further exposure to sevoflurane or isoflurane(1 minimal alveolar concentration ) for 60 minutes.
RESULTS:In ARDSp, sevoflurane reduced IL-6 expression to a greater degree than isoflurane (P = .04). Static lung elastance (P = .0049) and alveolar collapse (P = .033) were lower in sevoflurane than isoflurane, whereas Nrf2 (P = .036), SP-B (P = .042), and β1-Na,K-ATPase (P = .038) expressions were higher in sevoflurane. In ARDSexp, no significant differences were observed in lungmechanics, alveolar collapse, or molecular parameters between sevoflurane and isoflurane. In vitro, SP-B expression was higher insevoflurane than isoflurane (P = .026).
CONCLUSIONS:Compared with isoflurae, sevoflurane did not
affect lung inflammation in ARDSexp, but it did reduce lunginflammation in ARDSp.
麻醉学文献进展分享
联系我们