The effect of exercise on the oxidative stress induced by experimental lung injury.

AIM: The effects of physical exercise on oxidative stress parameters and immunocontent of NF-кß/p65 in lung of rats submitted to lung injury, as well as its possible protective effect on the changes in the alveolar-capillary barrier (total cell count, lactate dehydrogenase and total protein) in the bronchoalveolar lavage fluid (BALF) and the inflammatory infiltration in the pulmonary parenchyma were evaluated. MAIN METHODS: Wistar rats were submitted to two months of physical exercise and after this period, lung injury was induced by intratracheal instillation of lipopolysaccharide (dose of 100 µg/100 g body weight). Twelve hours after injury, the animals were sacrificed and lung and BALF were collected. KEY FINDINGS: Results showed an increase in reactive species production, lipid peroxidation, oxidative damage to protein, as well as in nitrite levels and NF-кß/p65 immunocontent in lung of rats submitted to lung injury. Physical exercise was able to totally prevent the increase in reactive species, nitrite levels and NF-кß/p65 immunocontent, but partially prevented the damage to protein. Superoxide dismutase and catalase were not changed in lung injury group, but the activities of these enzymes were increased in lung injury plus exercise group. Non-enzymatic antioxidant capacity, glutathione content and glutathione peroxidase were decreased and exercise totally prevented such effects. Rats subjected to lung injury presented an increase in total cell, lactate dehydrogenase and total protein; exercise partially prevented the increase in lactate dehydrogenase. SIGNIFICANCE: These findings suggest that physical exercise may prevent, at least partially, the oxidative damage caused by experimental lung injury, suggesting that exercise may have an important role as protector in this condition.

Entendendo a estrutura microscópica e submicroscópica da barreira alvéolo-capilar na lesão pulmonar aguda / Understanding the microscopic and submicroscopic structure of the alveolar-capillary membrane in acute lung injury

A lesão pulmonar aguda/síndrome do desconforto respiratório agudo (LPA/SDRA) pode ser induzida por diferentes causas. A lesão pulmonar ocorre por efeito direto sobre as células epiteliais pulmonares ou em decorrência de efeito indireto sobre as células endoteliais, onde o dano pulmonar decorre da liberação de mediadores inflamatórios em órgãos distais. Neste artigo, enfatizamos as diferenças microscópicas e submicroscópicas no pulmão envolvido na LPA e SDRA, ambas caracterizadas por intensa resposta inflamatória local com acúmulo de diferentes tipos celulares.O remodelamento do parênquima pulmonar caracterizado por fibroelastogênese ocorre em paralelo com o processo inflamatório. O prognóstico do paciente dependerá da resolução do evento inicial e do balanço entre a intensidade das respostas inflamatória e de remodelamento. Diferentes protocolos tentam modificar ambas as respostas, mas todos com resultados negativos. Postulamos que, para uma melhor compreensão da fisiopatologia da SDRA, diferenças microscópicas e submicroscópicas devem ser consideradas. Logo, para se estabelecer uma conduta clínica mais precisa e melhorar o prognóstico desses pacientes, deve-se considerar a etiologia da LPA/SDRA.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) can be induced by various causes. Lung injury can occur through direct or indirect effects on the lung epithelial cells, the latter caused by the release of inflammatory mediators in distal organs. In this article, we emphasize the lung microscopy and ultrastructural changes seen in ALI and ARDS, both of which are characterized by an intense inflammatory process with cell infiltration. The lung parenchyma remodeling process is characterized by fibroelastogenesis occurring in parallel with the inflammatory process. The prognosis depends on the resolution of the initial event and on the balance between the inflammatory response and the remodeling process. Although various protocols have been developed in attempts to modify those aspects, none have produced positive results.We postulate that a better understanding of ARDS cannot be gained without taking lung microscopy and ultrastructural analysis of the lung parenchyma into account. Therefore, in order to improve the clinical management and the prognosis of patients with ALI/ARDS, the etiology of the syndrome should be considered.