呼气末正压和肺复张策略在呼吸机相关性损伤小鼠模型中的作用
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Effects of positive end-expiratory pressure and recruitment maneuvers in a ventilator induced injury mouse model
背景与目的
正压通气是临床上重要的治疗手段，但却导致了呼吸机相关性肺损伤的临床症状出现。肺保护性机械通气策略各有不同，但都旨在减少或防止呼吸机相关性肺损伤。然而，少有策略被证明有效。为了更好地了解导致呼吸机相关性肺损伤的生物学机制，需要隔离出机械通气模型来探讨它在急性肺损伤发展中的作用。
方 法
5-12周龄的雌性BALB/c小鼠（n = 85）进行麻醉，机械通气2h或4h，潮气量选择小潮气量（8ml/kg）或大潮气量（15ml/kg），有或无呼气末正压通气和肺复张。
结 果
大潮气量组通气2h时肺泡毛细血管屏障发生改变，大潮气量组在4h通气时，组织学评分、支气管肺泡灌洗液白蛋白、炎性细胞因子和中性粒细胞浓度明显升高。在大和小潮气量通气组呼气末正压的应用显著减少了标准化组织学评分和支气管肺泡中性粒细胞绝对计数。在2h和4h机械通气中，肺复张是维持肺顺应性必需的。
结 论
呼吸机相关性肺损伤的征象在大通气量组很明显（2小时即可发生），且长期通气（4小时）时肺损伤加重。呼气末正压和肺复张应用在所有时间点都有对抗VILI进展的作用。动态顺应性可用于指导肺复张应用的频率来改
善机械通气所致肺损伤。
原始文献摘要
Cagle L A, Franzi L M, Linderholm A L, et al. Effects of positive end-expiratory pressure and recruitment maneuvers in a ventilator-induced injury mouse model[J]. Plos One, 2017, 12(11):e0187419.
Background：Positive-pressure mechanical ventilation is an essential therapeutic intervention, yet it causes the clinical syndrome known as ventilator-induced lung injury. Various lung protective mechanical ventilation strategies have attempted to reduce or prevent ventilator[1]induced lung injury but few modalities have proven effective. A model that isolates the contribution of mechanical ventilation on the development of acute lung injury is needed to better understand biologic mechanisms that lead to ventilator-induced lung injury.
Objectives：To evaluate the effects of positive end-expiratory pressure and recruitment maneuvers in reducing lung injury in a ventilator-induced lung injury murine model in short- and longer-term ventilation.
Methods：5-12 week-old female BALB/c mice (n = 85) were anesthetized, placed on mechanical ventilation for either 2 hrs or 4 hrs with either low tidal volume (8 ml/kg) or high tidal volume (15ml/kg) with or without positive end-expiratory pressure and recruitment maneuvers.
Results：Alteration of the alveolar-capillary barrier was noted at 2 hrs of high tidal volume ventilation.Standardized histology scores, influx of bronchoalveolar lavage albumin, proinflammatory cytokines, and absolute neutrophils were significantly higher in the high-tidal volume ventilation group at 4 hours of ventilation. Application of positive end-expiratory pressure resulted in significantly decreased standardized histology scores and bronchoalveolar absoluteneutrophil counts at low- and high-tidal volume ventilation, respectively. Recruitment maneuvers were essential to maintain pulmonary compliance at both 2 and 4 hrs of ventilation.
Conclusions：Signs of ventilator-induced lung injury are evident soon after high tidal volume ventilation (as early as 2 hours) and lung injury worsens with longer-term ventilation (4 hrs). Application of positive end-expiratory pressure and recruitment maneuvers are protective against worsening VILI across all time points. Dynamic compliance can be used guide the frequency of recruitment maneuvers to help ameliorate ventilator-induced lung injury.
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