Whitehead Thomas C, Zhang Haibo, Mullen Brendan, Slutsky Arthur S
Departments of Anesthesia and Critical Care Medicine, St Michael's Hospital, University of Toronto, Canada.
Anesthesiology. 2004 Jul;101(1):52-8. doi: 10.1097/00000542-200407000-00010.
Mechanical ventilation may cause lung injury through the excitation of an inflammatory response and the release of mediators, such as cytokines. The authors tested the hypothesis that intratracheal lipopolysaccharide amplifies the cytokine response to mechanical ventilation.
Rat lungs were intratracheally instilled with lipopolysaccharide followed by ex vivo mechanical ventilation for 2 h with low tidal volume of 7 ml/kg with 3 cm H2O positive end-expiratory pressure (PEEP), high tidal volume of 40 ml/kg with zero PEEP, medium tidal volume of 15 ml/kg with 3 cm H2O PEEP, or medium tidal volume and zero PEEP.
In the absence of lipopolysaccharide, lung lavage concentrations of tumor necrosis factor and interleukin 1 beta but not macrophage inflammatory protein 2 were significantly higher in lungs ventilated at high tidal volume/zero PEEP than at low tidal volume. There was a marked increase in lavage tumor necrosis factor and macrophage inflammatory protein 2 concentrations in lungs ventilated at low tidal volume after exposure to intratracheal lipopolysaccharide at doses of 100 ng/ml or greater. However, in lungs ventilated at high tidal volume, this response to lipopolysaccharide was markedly reduced. In addition, the number of alveolar macrophages recovered in the lavage was significantly lower in lungs ventilated at high tidal volume.
Ventilation strategy can modify lung cytokine responses to lipopolysaccharide, likely through an effect on the alveolar macrophage population.
机械通气可能通过激发炎症反应和释放细胞因子等介质而导致肺损伤。作者检验了气管内注入脂多糖会放大对机械通气的细胞因子反应这一假设。
给大鼠肺内气管内注入脂多糖，然后进行体外机械通气2小时，潮气量分别为7毫升/千克（呼气末正压3厘米水柱）、40毫升/千克（呼气末正压为零）、15毫升/千克（呼气末正压3厘米水柱）或15毫升/千克（呼气末正压为零）。
在没有脂多糖的情况下，大潮气量/零呼气末正压通气的肺灌洗中肿瘤坏死因子和白细胞介素1β的浓度显著高于小潮气量通气的肺，但巨噬细胞炎性蛋白2的浓度并非如此。在气管内注入100纳克/毫升或更高剂量脂多糖后，小潮气量通气的肺灌洗中肿瘤坏死因子和巨噬细胞炎性蛋白2的浓度显著增加。然而，大潮气量通气的肺对脂多糖的这种反应明显减弱。此外，大潮气量通气的肺灌洗中回收的肺泡巨噬细胞数量显著减少。
通气策略可能通过对肺泡巨噬细胞群体的影响来改变肺对脂多糖的细胞因子反应。
