咪达唑仑镇静比右美托咪定和丙泊酚更加抑制机械通气大鼠膈肌功能
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咪达唑仑镇静比右美托咪定和丙泊酚更加抑制机械通气大鼠膈肌功能
翻译：冯玉蓉 编辑：冯玉蓉 审校：曹莹
背景：机械通气（MV）被认为是膈肌萎缩和收缩功能障碍的独立因素。适当的镇静在MV期间是必要的，麻醉可能对膈肌有直接的不良影响。然而，对于MV期间不同麻醉药物对膈肌功能的影响，目前还缺乏相关研究。
目的：本研究旨在探讨咪达唑仑、右美托咪定和丙泊酚在MV期间对膈肌功能的影响。
设计：动物实验。
单位：大学研究实验室。
实验对象：雄性Wistar大鼠。
干预措施：在持续输注麻醉药的情况下，大鼠进行12小时的MV或自主呼吸（SB）。检测膈肌收缩特性、横截面积、微循环、氧化应激和蛋白水解情况。
测量方法和主要结果：MV后，与右美托咪定组（−60.4±3.01%，p<0.001）和丙泊酚组（−58.3±2.60%，p<0.001）相比，咪达唑仑组的膈肌比力显著降低。与右美托咪定（−21.8±2.11%，p=0.0001）和丙泊酚（−8.2±1.53%，p=0.003）相比，MV期间用咪达唑仑镇静会引起更多的II型纤维萎缩。在SB条件下，咪达唑仑组、右美托咪定组和丙泊酚组的上述指标无显著性差异（所有p>0.05）。12小时的MV导致膈肌功能性毛细血管密度随时间变化而降低（PB −25.1%, p = 0.0001; MZ −21.6%, p = 0.0003; DD −15.2%, p = 0.022; PP −24.8%, p = 0.0001），但在腓肠肌中并未发生此类情况。右美托咪定组和丙泊酚组的膈肌脂质过氧化加合物4-HNE和HIF-1α水平均显著低于咪达唑仑组（p<0.05）。同时，与右美托咪定组和丙泊酚组相比，咪达唑仑组的过氧化氢酶和SOD水平也相对较低（p<0.05）。
结论：机械通气12小时期间，咪达唑仑镇静导致的膈肌功能障碍比右美托咪定和丙泊酚更严重，可能是由于咪达唑仑抗氧化能力相对较弱所致。
Sedation with midazolam worsens the diaphragm function than dexmedetomidine and propofol during mechanical ventilation in rats
Abstract
Background: Mechanical ventilation (MV) is identified as an independent contributor to diaphragmatic atrophy and contractile dysfunction. Appropriate sedation is also essential during MV, and anesthetics may have direct adverse effects on the diaphragm. However, there is a lack of research into the effects of different anesthetics on diaphragm function during MV.
Objectives: In the present study, we aim to examine the effect of midazolam, dexmedetomidine, and propofol on diaphragm function during MV.
Design: Animal study.
Setting: University research laboratory.
Subjects: Male Wistar rats.
Interventions: Animals were experienced 12 h of MV or spontaneous breathing (SB) with continuous anesthetics infusion. Diaphragm contractile properties, cross-sectional areas, microcirculation, oxidative stress, and proteolysis were examined.
Measurements and main results: Diaphragmatic specific force was markedly reduced in the midazolam group compared with the dexmedetomidine (−60.4 ± 3.01%, p < 0.001) and propofol group (−58.3 ± 2.60%, p < 0.001) after MV. MV sedated with midazolam induced more atrophy of type II fibers compared with dexmedetomidine (−21.8 ± 2.11%, p = 0.0001) and propofol (−8.2 ± 1.53%, p = 0.003). No significant differences of these indices were found in the midazolam, dexmedetomidine, and propofol groups under SB condition (all p > 0.05, respectively). Twelve hours of MV resulted in a time dependent reduction in diaphragmatic functional capillary density (PB −25.1%, p = 0.0001; MZ −21.6%, p = 0.0003; DD −15.2%, p = 0.022; PP −24.8%, p = 0.0001, respectively), which did not occur in the gastrocnemius muscle. The diaphragmatic lipid peroxidation adducts 4-HNE and HIF-1α levels were significantly lower in dexmedetomidine group and propofol group compared to midazolam group (p < 0.05, respectively). Meanwhile, the catalase and SOD levels were also relatively lower (p < 0.05, respectively) in midazolam group compared to dexmedetomidine group and propofol group.
Conclusions: Twelve hours of mechanical ventilation during midazolam sedation led to a more severe diaphragm dysfunction than dexmedetomidine and propofol, possibly caused by its relative weaker antioxidant capacity.
贵州医科大学高鸿教授课题组
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