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首页> 外文期刊>American Journal of Physiology >Mechanical ventilation with moderate tidal volumes synergistically increases lung cytokine response to systemic endotoxin.
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Mechanical ventilation with moderate tidal volumes synergistically increases lung cytokine response to systemic endotoxin.

机译：具有中等潮气量的机械通气可协同增加肺细胞因子对全身内毒素的反应。

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Previous animal studies have identified a role for activation of innate immunity in the pathogenesis of ventilator-associated lung injury. These studies have used large tidal volume ventilation to study the effect of alveolar overdistension on induction of inflammatory pathways. We hypothesized an alternative mechanism for the pathogenesis of lung injury in which moderate tidal volume ventilation does not independently cause clinical inflammation but rather interacts with innate immune activation by bacterial products, resulting in an enhanced inflammatory response. We measured cytokine expression and lung injury in normal and lipopolysaccharide (LPS)-treated anesthetized rabbits randomized to either spontaneous respiration or mechanical ventilation. Outcome parameters were analyzed by two-way factorial analysis of variance to identify synergism between ventilation and systemic LPS. Mechanical ventilation alone resulted in minimal cytokine expression in the lung but did enhance LPS-induced expression of tumor necrosis factor-alpha, the CXC chemokines interleukin-8 and growth-related protein-alpha, and the CC chemokine monocyte chemoattractant protein-1. Increased mRNA expression and activation of the transcription factors nuclear factor-kappaB and activator protein-1 accompanied the cytokine responses. We conclude that moderate volume ventilation strategies augment the innate immune response to bacterial products in the lung and may play a role in the development of acute lung injury in patients with sepsis.
机译：先前的动物研究已经确定了在呼吸机相关性肺损伤的发病机理中激活先天免疫的作用。这些研究使用大潮气量通气来研究肺泡过度扩张对炎症途径的诱导作用。我们假设了肺损伤发病机制的另一种机制，其中适度的潮气量通气不会独立引起临床炎症，而是与细菌产物的先天免疫激活相互作用，从而导致炎症反应增强。我们测量了随机和自发呼吸或机械通气的正常和脂多糖（LPS）处理的麻醉兔的细胞因子表达和肺损伤。结果结果参数通过方差的双向分析进行分析，以确定通气与系统性LPS之间的协同作用。单独的机械通气导致肺中最小的细胞因子表达，但确实增强了LPS诱导的肿瘤坏死因子-α，CXC趋化因子白细胞介素8和生长相关蛋白-α以及CC趋化因子单核细胞趋化蛋白1的表达。 mRNA表达的增加和转录因子核因子-κB和激活蛋白-1的激活伴随着细胞因子的反应。我们得出结论，适量的通气策略可增强对肺部细菌产物的先天免疫反应，并可能在脓毒症患者急性肺损伤的发生中发挥作用。

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