低强度游泳训练部分抑制脂多糖诱导的急性肺损伤。

Low-intensity swimming training partially inhibits lipopolysaccharide-induced acute lung injury.

机构信息

Laboratory of Physiology and Pharmacodynamics, Institute of Research and Development, University of Vale do Paraíba, Săo Paulo, Brazil.

出版信息

Med Sci Sports Exerc. 2010 Jan;42(1):113-9. doi: 10.1249/MSS.0b013e3181ad1c72.

DOI:10.1249/MSS.0b013e3181ad1c72

PMID:20010123

Abstract

BACKGROUND

Aerobic exercise decreases pulmonary inflammation and remodeling in experimental models of allergic asthma. However, the effects of aerobic exercise on pulmonary inflammation of nonallergic origin, such as in experimental models of acute lung injury induced by lipopolysaccharide (LPS), have not been evaluated.

OBJECTIVE

The present study evaluated the effects of aerobic exercise in a model of LPS-induced acute lung injury.

METHODS

BALB/c mice were divided into four groups: Control, Aerobic Exercise, LPS, and Aerobic Exercise + LPS. Swimming tests were conducted at baseline and at 3 and 6 wk. Low-intensity swimming training was performed for 6 wk, four times per week, 60 min per session. Intranasal LPS (1 mg x kg(-1) (60 microg per mouse)) was instilled 24 h after the last swimming physical test in the LPS and Aerobic Exercise + LPS mice, and the animals were studied 24 h after LPS instillation. Exhaled nitric oxide, respiratory mechanics, total and differential cell counts in bronchoalveolar lavage, and lung parenchymal inflammation and remodeling were evaluated.

RESULTS

LPS instillation resulted in increased levels of exhaled nitric oxide (P < 0.001), higher numbers of neutrophils in the bronchoalveolar lavage (P < 0.001) and in the lung parenchyma (P < 0.001), and decreased lung tissue resistance (P < 0.05) and volume proportion of elastic fibers (P < 0.01) compared with the Control group. Swim training in LPS-instilled animals resulted in significantly lower exhaled nitric oxide levels (P < 0.001) and fewer neutrophils in the bronchoalveolar lavage (P < 0.001) and the lung parenchyma (P < 0.01) compared with the LPS group.

CONCLUSIONS

These results suggest that low-intensity swimming training inhibits lung neutrophilic inflammation, but not remodeling and impaired lung mechanics, in a model of LPS-induced acute lung injury.

摘要

背景

有氧运动可减少实验性变应性哮喘模型中的肺部炎症和重塑。然而，有氧运动对非变应原性起源的肺部炎症的影响，例如脂多糖（LPS）诱导的急性肺损伤实验模型，尚未得到评估。

目的

本研究评估了有氧运动在 LPS 诱导的急性肺损伤模型中的作用。

方法

BALB/c 小鼠分为 4 组：对照组、有氧运动组、LPS 组和有氧运动+LPS 组。在基线和第 3 周和第 6 周进行游泳测试。低强度游泳训练每周进行 4 次，每次 60 分钟，持续 6 周。在 LPS 和有氧运动+LPS 小鼠的最后一次游泳体能测试后 24 小时，经鼻内给予 LPS（1 mg x kg(-1)（每只小鼠 60 μg）），并在 LPS 给药后 24 小时对动物进行研究。评估呼气一氧化氮、呼吸力学、支气管肺泡灌洗液中的总细胞和分类细胞计数以及肺实质炎症和重塑。

结果

LPS 给药导致呼气一氧化氮水平升高（P < 0.001）、支气管肺泡灌洗液（P < 0.001）和肺实质（P < 0.001）中的中性粒细胞数量增加，肺组织阻力降低（P < 0.05）和弹性纤维体积比例降低（P < 0.01）与对照组相比。在 LPS 给药的动物中进行游泳训练导致呼气一氧化氮水平显著降低（P < 0.001），支气管肺泡灌洗液（P < 0.001）和肺实质（P < 0.01）中的中性粒细胞数量减少。