在脂多糖诱发急性肺损伤的实验模型中,机械通气过程中无电极区域对周围肺组织的影响。

Lídia Maria Carneiro Fonseca, Maycon Moura Reboredo, Leda Marília Fonseca Lucinda, Thaís Fernanda Fazza, Bruno Curty Bergamini, Mateus Pinto Botelho, Gabriele Moura Lopes, Juliana Dias Nascimento Ferreira, Erich Vidal Carvalho, Bruno Valle Pinheiro
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引用次数: 0

摘要

目的在脂多糖诱导的急性肺损伤大鼠无肺泡模型中,评估机械通气时无肺泡对肺泡周围和正常肺区的影响:将24只大鼠随机分为以下四组,每组6只:生理盐水对照组、脂多糖对照组、生理盐水偏流组和脂多糖偏流组。腹腔注射脂多糖诱发急性肺损伤。24 小时后,通过阻断支气管诱发肺不张。动物在保护参数下接受机械通气两小时,并在此期间监测呼吸力学。之后,对两个相关区域,即偏瘫周围区域和偏瘫区域对侧的正常通气肺进行组织学分析:结果:脂多糖对照组的肺损伤评分(0.41 ± 0.13)明显高于生理盐水对照组(0.15 ± 0.51),P < 0.05。在盐水偏流组(0.44 ± 0.06 x 0.27 ± 0.74 p < 0.05)和脂多糖偏流组(0.56 ± 0.09 x 0.35 ± 0.04 p < 0.05),偏流周围区域的肺损伤评分均高于正常通气区域。结论:多糖偏流组(0.56±0.09)比盐水偏流组(0.44±0.06)偏流周围肺损伤评分更高:在使用保护性参数进行机械通气一段时间后,气胸可能会对周围组织造成损伤。其对先前受伤肺部的影响更为显著。
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Effects of atelectatic areas on the surrounding lung tissue during mechanical ventilation in an experimental model of acute lung injury induced by lipopolysaccharide.

Objective: To assess the effect of atelectasis during mechanical ventilation on the periatelectatic and normal lung regions in a model of atelectasis in rats with acute lung injury induced by lipopolysaccharide.

Methods: Twenty-four rats were randomized into the following four groups, each with 6 animals: the Saline-Control Group, Lipopolysaccharide Control Group, Saline-Atelectasis Group, and Lipopolysaccharide Atelectasis Group. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide. After 24 hours, atelectasis was induced by bronchial blocking. The animals underwent mechanical ventilation for two hours with protective parameters, and respiratory mechanics were monitored during this period. Thereafter, histologic analyses of two regions of interest, periatelectatic areas and the normally-aerated lung contralateral to the atelectatic areas, were performed.

Results: The lung injury score was significantly higher in the Lipopolysaccharide Control Group (0.41 ± 0.13) than in the Saline Control Group (0.15 ± 0.51), p < 0.05. Periatelectatic regions showed higher lung injury scores than normally-aerated regions in both the Saline-Atelectasis (0.44 ± 0.06 x 0.27 ± 0.74 p < 0.05) and Lipopolysaccharide Atelectasis (0.56 ± 0.09 x 0.35 ± 0.04 p < 0.05) Groups. The lung injury score in the periatelectatic regions was higher in the Lipopolysaccharide Atelectasis Group (0.56 ± 0.09) than in the periatelectatic region of the Saline-Atelectasis Group (0.44 ± 0.06), p < 0.05.

Conclusion: Atelectasis may cause injury to the surrounding tissue after a period of mechanical ventilation with protective parameters. Its effect was more significant in previously injured lungs.

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