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Negative pressure ventilation and positive pressure ventilation promote comparable levels of ventilator-induced diaphragmatic dysfunction in rats

机译:负压通气和正压通气可促进同等水平的呼吸机诱发的comparable肌功能障碍

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BACKGROUND:: Mechanical ventilation is a life-saving intervention for patients with respiratory failure. Unfortunately, a major complication associated with prolonged mechanical ventilation is ventilator-induced diaphragmatic atrophy and contractile dysfunction, termed ventilator-induced diaphragmatic dysfunction (VIDD). Emerging evidence suggests that positive pressure ventilation (PPV) promotes lung damage (ventilator-induced lung injury [VILI]), resulting in the release of signaling molecules that foster atrophic signaling in the diaphragm and the resultant VIDD. Although a recent report suggests that negative pressure ventilation (NPV) results in less VILI than PPV, it is unknown whether NPV can protect against VIDD. Therefore, the authors tested the hypothesis that compared with PPV, NPV will result in a lower level of VIDD. METHODS:: Adult rats were randomly assigned to one of three experimental groups (n = 8 each): (1) acutely anesthetized control (CON), (2) 12 h of PPV, and (3) 12 h of NPV. Dependent measures included indices of VILI, diaphragmatic muscle fiber cross-sectional area, diaphragm contractile properties, and the activity of key proteases in the diaphragm. RESULTS:: Our results reveal that no differences existed in the degree of VILI between PPV and NPV animals as evidenced by VILI histological scores (CON = 0.082 ± 0.001; PPV = 0.22 ± 0.04; NPV = 0.25 ± 0.02; mean ± SEM). Both PPV and NPV resulted in VIDD. Importantly, no differences existed between PPV and NPV animals in diaphragmatic fiber cross-sectional area, contractile properties, and the activation of proteases. CONCLUSION:: These results demonstrate that NPV and PPV result in similar levels of VILI and that NPV and PPV promote comparable levels of VIDD in rats.
机译:背景:机械通气是呼吸衰竭患者的一种救生干预措施。不幸的是,与长时间机械通气有关的主要并发症是呼吸机诱发的diaphragm肌萎缩和收缩功能障碍,称为呼吸机诱发的diaphragm肌功能障碍(VIDD)。越来越多的证据表明,正压通气(PPV)会促进肺部损伤(呼吸机诱发的肺损伤[VILI]),导致释放促进隔膜中萎缩性信号传导的信号分子以及由此产生的VIDD。尽管最近的一份报告表明负压通气(NPV)导致的VILI低于PPV,但尚不清楚NPV是否可以预防VIDD。因此,作者检验了以下假设:与PPV相比,NPV会导致VIDD水平降低。方法:成年大鼠被随机分为三个实验组(每组8只)之一:(1)急性麻醉对照组(CON),(2)PPV 12小时和(3)NPV 12小时。相关指标包括VILI指数,diaphragm肌纤维横截面积,diaphragm肌收缩特性以及diaphragm肌中关键蛋白酶的活性。结果:我们的研究结果表明,通过VILI组织学评分(CON = 0.082±0.001; PPV = 0.22±0.04; NPV = 0.25±0.02;平均值±SEM),PPV和NPV动物之间的VILI程度没有差异。 PPV和NPV均导致VIDD。重要的是,PPV和NPV动物之间在横隔膜纤维横截面积,收缩特性和蛋白酶激活方面没有差异。结论:这些结果表明NPV和PPV导致相似的VILI水平,并且NPV和PPV促进了大鼠中相当水平的VIDD。

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