Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Centro de Ciências da Saúde, Rio de Janeiro, Brazil.
Br J Anaesth. 2016 May;116(5):708-15. doi: 10.1093/bja/aew093.
Variable ventilation improves respiratory function, but it is not known whether the amount of variability in tidal volume (VT) can be reduced in recruited lungs without a deterioration of respiratory system elastance.
Acute lung inflammation was induced by intratracheal instillation of lipopolysaccharide in 35 Wistar rats. Twenty-eight animals were anaesthetized and ventilated in volume-controlled mode. Lungs were recruited by random variation of VT (mean 6 ml kg(-1), coefficient of variation 30%, normal distribution) for 30 min. Animals were randomly assigned to different amounts of VT variability (n=7 for 90 min per group): 30, 15, 7.5, or 0%. Lung function, diffuse alveolar damage, and gene expression of biological markers associated with cell mechanical stress, inflammation, and fibrogenesis were assessed. Seven animals were not ventilated and served as controls for post-mortem analyses.
A VT variability of 30%, but not 15, 7.5, or 0%, prevented deterioration of respiratory system elastance [Mean (SD) -7.5 (8.7%), P<0.05; 21.1 (9.6%), P<0.05; 43.3 (25.9), P<0.05; and 41.2 (16.4), P<0.05, respectively]. Diffuse alveolar damage was lower with a VT variability of 30% than with 0% and without ventilation, because of reduced oedema and haemorrhage. A VT variability of 30, 15, or 7.5% reduced the gene expression of amphiregulin, cytokine-induced neutrophil chemoattractant-1, and tumour necrosis factor α compared with a VT variability of 0%.
In this model of acute lung inflammation, a VT variability of 30%, compared with 15 and 7.5%, was necessary to avoid deterioration of respiratory system elastance and was not associated with lung histological damage.
可变通气可以改善呼吸功能,但尚不清楚在募集的肺中是否可以减少潮气量(VT)的变化量,而不会使呼吸系统弹性恶化。
通过气管内滴注脂多糖在 35 只 Wistar 大鼠中诱导急性肺炎症。28 只动物在容量控制模式下麻醉并通气。通过 VT 的随机变化(平均 6ml/kg,变异系数 30%,正态分布)募集肺 30 分钟。动物被随机分配到不同的 VT 变化量(每组 7 只):30、15、7.5 或 0%。评估肺功能、弥漫性肺泡损伤以及与细胞机械应激、炎症和纤维化相关的生物标志物的基因表达。7 只动物未通气,作为死后分析的对照。
VT 变异性为 30%,但不是 15%、7.5%或 0%,可防止呼吸系统弹性的恶化[-7.5(8.7%),P<0.05;21.1(9.6%),P<0.05;43.3(25.9%),P<0.05;和 41.2(16.4%),P<0.05,分别]。由于水肿和出血减少,与 0%和无通气相比,30%的 VT 变异性导致弥漫性肺泡损伤降低。与 0%相比,30%、15%或 7.5%的 VT 变异性降低了 Amphiregulin、细胞因子诱导的中性粒细胞趋化因子-1 和肿瘤坏死因子α的基因表达。
在这种急性肺炎症模型中,与 15%和 7.5%相比,30%的 VT 变异性可避免呼吸系统弹性的恶化,并且与肺组织学损伤无关。