Moraes Lillian, Santos Cíntia Lourenco, Santos Raquel Souza, Cruz Fernanda Ferreira, Saddy Felipe, Morales Marcelo Marcos, Capelozzi Vera Luiza, Silva Pedro Leme, de Abreu Marcelo Gama, Garcia Cristiane Sousa Nascimento Baez, Pelosi Paolo, Rocco Patricia Rieken Macedo
Crit Care. 2014 Aug 12;18(4):474. doi: 10.1186/s13054-014-0474-4.
Sigh improves oxygenation and lung mechanics during pressure control ventilation (PCV) and pressure support ventilation (PSV) in patients with acute respiratory distress syndrome. However, so far, no study has evaluated the biological impact of sigh during PCV or PSV on the lung and distal organs in experimental pulmonary (p) and extrapulmonary (exp) mild acute lung injury (ALI).
In 48 Wistar rats, ALI was induced by Escherichia coli lipopolysaccharide either intratracheally (ALIp) or intraperitoneally (ALIexp). After 24 hours, animals were anesthetized and mechanically ventilated with PCV or PSV with a tidal volume of 6 mL/kg, FiO2 = 0.4, and PEEP = 5 cmH2O for 1 hour. Both ventilator strategies were then randomly assigned to receive periodic sighs (10 sighs/hour, Sigh) or not (non-Sigh, NS). Ventilatory and mechanical parameters, arterial blood gases, lung histology, interleukin (IL)-1β, IL-6, caspase-3, and type III procollagen (PCIII) mRNA expression in lung tissue, and number of apoptotic cells in lung, liver, and kidney specimens were analyzed.
In both ALI etiologies: (1) PCV-Sigh and PSV-Sigh reduced transpulmonary pressure, and (2) PSV-Sigh reduced the respiratory drive compared to PSV-NS. In ALIp: (1) PCV-Sigh and PSV-Sigh decreased alveolar collapse as well as IL-1β, IL-6, caspase-3, and PCIII expressions in lung tissue, (2) PCV-Sigh increased alveolar-capillary membrane and endothelial cell damage, and (3) abnormal myofibril with Z-disk edema was greater in PCV-NS than PSV-NS. In ALIexp: (1) PSV-Sigh reduced alveolar collapse, but led to damage to alveolar-capillary membrane, as well as type II epithelial and endothelial cells, (2) PCV-Sigh and PSV-Sigh increased IL-1β, IL-6, caspase-3, and PCIII expressions, and (3) PCV-Sigh increased the number of apoptotic cells in the lung compared to PCV-NS.
In these models of mild ALIp and ALIexp, sigh reduced alveolar collapse and transpulmonary pressures during both PCV and PSV; however, improved lung protection only during PSV in ALIp.
在急性呼吸窘迫综合征患者的压力控制通气（PCV）和压力支持通气（PSV）过程中，叹息可改善氧合及肺力学。然而，迄今为止，尚无研究评估在实验性肺（p）和肺外（exp）轻度急性肺损伤（ALI）中，PCV或PSV期间叹息对肺及远端器官的生物学影响。
在48只Wistar大鼠中，通过气管内（ALIp）或腹腔内（ALIexp）注射大肠杆菌脂多糖诱导ALI。24小时后，将动物麻醉并采用PCV或PSV进行机械通气，潮气量为6 mL/kg，FiO2 = 0.4，呼气末正压（PEEP）= 5 cmH2O，持续1小时。然后将两种通气策略随机分为接受周期性叹息（每小时10次叹息，叹息组）或不接受（非叹息组，NS）。分析通气和力学参数、动脉血气、肺组织学、白细胞介素（IL）-1β、IL-6、半胱天冬酶-3和III型前胶原（PCIII）在肺组织中的mRNA表达，以及肺、肝和肾标本中的凋亡细胞数量。
在两种ALI病因中：（1）PCV-叹息组和PSV-叹息组降低了跨肺压，（2）与PSV-NS相比，PSV-叹息组降低了呼吸驱动。在ALIp中：（1）PCV-叹息组和PSV-叹息组减少了肺泡萎陷以及肺组织中IL-1β、IL-6、半胱天冬酶-3和PCIII的表达，（2）PCV-叹息组增加了肺泡-毛细血管膜和内皮细胞损伤，（3）PCV-NS组中具有Z盘水肿的异常肌原纤维比PSV-NS组更严重。在ALIexp中：（1）PSV-叹息组减少了肺泡萎陷，但导致肺泡-毛细血管膜以及II型上皮和内皮细胞损伤，（2）PCV-叹息组和PSV-叹息组增加了IL-1β、IL-6、半胱天冬酶-3和PCIII的表达，（3）与PCV-NS相比，PCV-叹息组增加了肺中凋亡细胞的数量。
在这些轻度ALIp和ALIexp模型中，叹息在PCV和PSV期间均降低了肺泡萎陷和跨肺压；然而，仅在ALIp的PSV期间改善了肺保护。
