1 Chest Department, Taipei Veterans General Hospital, Taipei 112, Taiwan.
2 Institutes of Clinical Medicine, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan.
Exp Biol Med (Maywood). 2018 Dec;243(17-18):1329-1337. doi: 10.1177/1535370218811950. Epub 2018 Nov 19.
Mechanical ventilation (MV) is life-saving for patients with acute respiratory failure but also causes difficult liberation of patients from ventilator due to rapid decrease of diaphragm muscle endurance and strength, which is termed ventilator-induced diaphragmatic damage (VIDD). Numerous studies have revealed that VIDD could increase extubation failure, ICU stay, ICU mortality, and healthcare expenditures. However, the mechanisms of VIDD, potentially involving a multistep process including muscle atrophy, oxidative loads, structural damage, and muscle fiber remodeling, are not fully elucidated. Further research is necessary to unravel mechanistic framework for understanding the molecular mechanisms underlying VIDD, especially mitochondrial dysfunction and increased mitochondrial oxidative stress, and develop better MV strategies, rehabilitative programs, and pharmacologic agents to translate this knowledge into clinical benefits.
机械通气（MV）是急性呼吸衰竭患者的救命手段，但也会由于膈肌肌肉耐力和力量迅速下降而导致患者难以脱离呼吸机，这被称为呼吸机诱导的膈肌损伤（VIDD）。大量研究表明，VIDD 会增加拔管失败、ICU 住院时间、ICU 死亡率和医疗保健支出。然而，VIDD 的机制，可能涉及包括肌肉萎缩、氧化负荷、结构损伤和肌纤维重塑在内的多步骤过程，尚未完全阐明。需要进一步的研究来揭示理解 VIDD 分子机制的机制框架，特别是线粒体功能障碍和增加的线粒体氧化应激，并开发更好的 MV 策略、康复计划和药物来将这些知识转化为临床益处。
