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首页> 外文期刊>Pulmonary pharmacology & therapeutics >Effect of surfactant on ventilation-induced mediator release in isolated perfused mouse lungs.
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Effect of surfactant on ventilation-induced mediator release in isolated perfused mouse lungs.

机译：表面活性剂对离体灌注小鼠肺中通气诱导的介质释放的影响。

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The human acute respiratory distress syndrome (ARDS) is a severe pulmonary complication with high mortality rates. To support their vital functions, patients suffering from ARDS are mechanically ventilated. Recently it was shown that low tidal volume ventilation reduces mortality and pro-inflammatory mediator release in these patients, suggesting biotrauma as a side effect of mechanical ventilation. Because the application of exogenous surfactant has been proposed as a treatment for ARDS, we investigated the effect of surfactant on ventilation-induced release of tumor necrosis factor (TNF), interleukin-6 (IL-6) and 6-keto-PGF(1 alpha) (the stable metabolite of prostacyclin) in isolated perfused mouse lungs ventilated with high end-inspiratory pressures. Instillation of 100mg/kg surfactant into the lungs was well tolerated and improved tidal volume, pulmonary compliance and alveolar expansion. Exogenous surfactant increased the ventilation-induced liberation of TNF and IL-6 into the perfusate, but had no effect on the release of 6-keto-PGF(1 alpha). The surfactant preparation used reduced baseline TNF production by murine alveolar macrophages, indicating that the exaggeration of ventilation-induced TNF release cannot be explained by a direct effect of surfactant on these cells. We hypothesize that ventilation-induced mediator release is explained by stretching of lung cells, which is reinforced by surfactant. The findings that in this model of ventilation-induced lung injury exogenous surfactant at the same time improved lung functions and enhanced mediator release suggest that surfactant treatment may prevent barotrauma and augment biotrauma.
机译：人类急性呼吸窘迫综合征（ARDS）是一种严重的肺部并发症，死亡率很高。为了维持其重要功能，患有ARDS的患者需要进行机械通气。最近显示，低潮气量通气可降低这些患者的死亡率和促炎介质的释放，提示生物创伤是机械通气的副作用。由于已提议使用外源性表面活性剂治疗ARDS，因此我们研究了表面活性剂对通气诱导的肿瘤坏死因子（TNF），白介素6（IL-6）和6-酮-PGF（1）释放的影响。 α）（前列环素的稳定代谢产物）在高吸气末压通气的离体灌注小鼠肺中。良好地耐受向肺中滴注100mg / kg表面活性剂，并改善了潮气量，肺顺应性和肺泡扩张。外源性表面活性剂增加通气诱导的TNF和IL-6释放到灌注液中，但对6-酮-PGF（1α）的释放没有影响。表面活性剂制剂使用的鼠肺泡巨噬细胞降低了基线TNF的产生，表明通气诱导的TNF释放的夸张不能用表面活性剂对这些细胞的直接作用来解释。我们假设通气诱导的介质释放是由肺细胞的拉伸解释的，而肺细胞的拉伸由表面活性剂增强。在这种通气诱发的肺损伤模型中，外源性表面活性剂同时改善了肺功能并增强了介质释放的发现表明，表面活性剂治疗可以预防气压伤并增加生物损伤。

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