不同通气方式对机械通气引起急性肺损伤兔模型的影响

Effects of different ventilatory strategies on ventilator induced lung injury: a study of a rabbit model of acute lung injury

目的：通过表面活性物质缺乏的兔肺模型，评估传统通气模式（ｃｏｎｖｅｎｔｉｏｎａｌ ｍｅｃｈａｎｉｃａｌ ｖｅｎｔｉｌａｔｉｏｎ，ＣＭＶ）与允许性高碳酸血症加最佳ＰＥＥＰ（ｐｅｒｍｉｓｓｉｖｅ ｈｙｐｅｒｃａｐｎｉａａｓｓｏｃｉａｔｅｄ ｗｉｔｈｉｄｅａｌＰＥＥＰｖｅｎｔｉｌａｔｉｏｎ，ＰＨＹ＋ ＰＥＥＰｉ）的通气模式对肺损伤的影响，了解肿瘤坏死因子α（ｔｕｍｏｒ ｎｅｃｒｏｓｉｓｆａｃｔｏｒα，ＴＮＦα） 与机械通气引起肺损伤（ｖｅｎｔｉｌａｔｏｒｉｎｄｕｃｅｄｌｕｎｇｉｎｊｕｒｙ，ＶＩＬＩ） 的关系。方法：１２ 只成年兔，以反复肺灌洗法制备表面活性物质缺乏兔肺模型。以ＣＭＶ（Ｃ组） 或ＰＨＹ＋ ＰＥＥＰｉ （Ｐ 组） 通气４ ｈ 后，测定通气前、后的支气管肺泡灌洗液（ｂｒｏｎｃｈｏａｌｖｅｏｌａｒ ｌａｖａｇｅ ｆｌｕｉｄ，ＢＡＬＦ）中ＴＮＦα含量和白细胞分类计数，测定肺水量，进行动脉血气分析和病理检查。结果：ＣＭＶ 组表现为明显的低氧血症，ＢＡＬＦ中较多的中性粒细胞数，总肺水量及血管外肺水量明显增多，肺内病理改变为较明显透明膜形成及炎性细胞聚集；而ＰＨＹ＋ ＰＥＥＰｉ 组引起较少的上述病理、生理变化。且ＣＭＶ 组ＢＡＬ?

Objective: To evaluate the influence of conventional mechanical ventilation (CMV) and permissive hypercapnia associated with ideal PEEP ventilation (PHY+PEEPi) on lung injury in surfactant depleted rabbit lungs, and to better understand the relationship between tumor necrosis factor α(TNFα) and ventilator induced lung injury. Methods: 12 anesthetized adult rabbits were tracheostomized, and surfactant depletion was induced by repeated saline lavage. Lung lavage for measurement of TNFα level was repeated after 4 h of CMV at FiO 2 of 1.0 or PHY+PEEPi at the same FiO 2. Arterial blood gas analysis, lavage cell counts and differential cytology, lung water measurement and pathological microscopic examination were performed. Results: Conventional mechanical ventilation (CMV) resulted in a progressive hypoxemia, increased number of neutrophils in bronchoalveolar lavage fluid (BALF), substantial morphological changes including hyaline membrane formation and neutrophils accumulation, increased total lung water (TLW) and extravascular lung water (EVLW) whereas PHY+PEEPi was associated with minimal changes in such physiological and pathological abnormalities. The levels of TNFα in lung lavage fluid were significantly greater in undergoing CMV than in undergoing PHY+PEEPi. Conclusion: The data suggest that CMV could result in much release of such inflammatory chemical mediator TNFα and much degree of lung injury than PHY+PEEPi, and that proinflammatory cytokines TNFα may play a pivotal role in ventilator induced lung injury.