Negative Pressure Ventilation and Positive Pressure Ventilation Promote Comparable Levels of Ventilator-induced Diaphragmatic Dysfunction in Rats
Negative Pressure Ventilation and Positive Pressure Ventilation Promote Comparable Levels of Ventilator-induced Diaphragmatic Dysfunction in Rats
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DOI：
10.1097/aln.0b013e31829b3692
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发表时间：
2013-09-01
期刊：
影响因子：
8.8
通讯作者：
Powers, Scott K.
中科院分区：
文献类型：
--
作者：
Bruells, Christian S.;Smuder, Ashley J.;Powers, Scott K.
背景：机械通气是呼吸衰竭患者的救命干预手段。不幸的是，与长时间机械通气相关的主要并发症是呼吸机诱发的膈肌萎缩和收缩功能障碍，称为呼吸机诱发的膈肌功能障碍（VIDD）。新出现的证据表明，正压通气（PPV）促进肺损伤（呼吸机诱导的肺损伤[VILI]），导致信号分子的释放，促进膈肌萎缩信号和由此产生的VIDD。尽管最近的一份报告表明，负压通气（NPV）导致的VILI比PPV少，但NPV是否能预防VIDD尚不清楚。因此，作者检验了与PPV相比，NPV会导致较低的VIDD水平的假设。方法：将成年大鼠随机分为3个实验组（每组8只）：(1)急性麻醉对照组（CON）， (2) PPV 12 h, (3) NPV 12 h。相关指标包括VILI、膈肌纤维横截面积、膈肌收缩特性和膈肌关键蛋白酶活性等指标。结果：通过VILI组织学评分（CON = 0.082 +/- 0.001; PPV = 0.22 +/- 0.04; NPV = 0.25 +/- 0.02；均数+/- SEM）， PPV和NPV动物的VILI程度没有差异。PPV和NPV都会导致VIDD。重要的是，PPV和NPV动物在膈纤维横截面积、收缩特性和蛋白酶激活方面没有差异。结论：NPV和PPV导致大鼠VILI水平相似，NPV和PPV促进VIDD水平相当。
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.