Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, ICBS, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, CEP 90035-003, Brazil.
Mol Cell Biochem. 2014 Apr;389(1-2):229-38. doi: 10.1007/s11010-013-1944-8. Epub 2013 Dec 31.
In the present study we investigated the effects of lung injury on energy metabolism (succinate dehydrogenase, complex II, cytochrome c oxidase, and ATP levels), respiratory mechanics (dynamic and static compliance, elastance and respiratory system resistance) in the lungs of rats, as well as on phospholipids in bronchoalveolar lavage fluid. The protective effect of physical exercise on the alterations caused by lung injury, including lung edema was also evaluated. Wistar rats were submitted to 2 months of physical exercise. After this period the lung injury was induced by intratracheal instillation of lipopolysaccharide. Adult Wistar rats were submitted to 2 months of physical exercise and after this period the lung injury was induced by intratracheal instillation of lipopolysaccharide in dose 100 μg/100 g body weight. The sham group received isotonic saline instillation. Twelve hours after the injury was performed the respiratory mechanical and after the rats were decapitated and samples were collected. The rats subjected to lung injury presented a decrease in activities of the enzymes of the electron transport chain and ATP levels in lung, as well as the formation of pulmonary edema. A decreased lung dynamic and static compliance, as well as an increase in respiratory system resistance, and a decrease in phospholipids content were observed. Physical exercise was able to totally prevent the decrease in succinate dehydrogenase and complex II activities and the formation of pulmonary edema. It also partially prevented the increase in respiratory system resistance, but did not prevent the decrease in dynamic and static compliance, as well as in phospholipids content. These findings suggest that the mitochondrial dysfunction may be one of the important contributors to lung damage and that physical exercise may be beneficial in this pathology, although it did not prevent all changes present in lung injury.
在本研究中,我们研究了肺损伤对大鼠肺能量代谢(琥珀酸脱氢酶、复合物 II、细胞色素 c 氧化酶和 ATP 水平)、呼吸力学(动态和静态顺应性、弹性和呼吸系统阻力)以及支气管肺泡灌洗液中磷脂的影响。还评估了体育锻炼对肺损伤引起的变化(包括肺水肿)的保护作用。Wistar 大鼠进行了 2 个月的体育锻炼。在此期间,通过气管内滴注脂多糖诱导肺损伤。成年 Wistar 大鼠进行了 2 个月的体育锻炼,然后通过气管内滴注 100μg/100g 体重的脂多糖诱导肺损伤。假手术组接受等渗盐水滴注。损伤后 12 小时进行呼吸力学检查,然后处死大鼠并收集样本。肺损伤大鼠的电子传递链酶活性和肺内 ATP 水平降低,同时发生肺水肿。观察到肺动态和静态顺应性降低,呼吸系统阻力增加,磷脂含量减少。体育锻炼能够完全预防琥珀酸脱氢酶和复合物 II 活性的降低和肺水肿的形成。它还部分预防了呼吸系统阻力的增加,但不能预防动态和静态顺应性以及磷脂含量的降低。这些发现表明,线粒体功能障碍可能是肺损伤的重要原因之一,而体育锻炼可能对这种病理有益,尽管它不能预防肺损伤中存在的所有变化。