Objective: To use an experimental model to evaluate the effect of heart failure on oxidative stress in the rat diaphragm. Methods: The model of myocardial infarction was developed through left coronary artery ligation. On day 42 after coronary artery ligation, the animals were killed, after which the diaphragms were collected and homogenized. Oxidative stress was evaluated in diaphragm homogenates through measurement of lipid peroxidation and assays of the activity of antioxidant enzymes, including catalase and glutathione peroxidase (enzymes that reduce hydrogen peroxide to water), as well as superoxide dismutase (an antioxidant enzyme that reduces superoxide anions to hydrogen peroxide). Results: The coronary artery ligation model was found to be effective in causing heart failure. In the animals submitted to coronary artery ligation, the mean infarcted area of the left ventricle was 39%. Lipid peroxidation was 217% greater in the diaphragms of ligated animals than in those of controls. The activity of catalase and glutathione peroxidase was 77% and 20% lower, respectively, in study rats than in control rats. Infarction did not modify superoxide dismutase activity. Conclusion: The results suggest that left coronary artery ligation results in oxidative stress in the diaphragm.

Keywords: Myocardial infarction; Oxidative stress; Congestive heart failure; Antioxidants; Diaphragm; Rats

Objective: To determine the effects of acute and chronic administration of methylprednisolone on oxidative stress, as quantified by measuring lipid peroxidation (LPO) and total reactive antioxidant potential (TRAP), in rat lungs. Methods: Forty Wistar rats were divided into four groups: acute treatment, comprising rats receiving a single injection of methylprednisolone (50 mg/kg i.p.); acute control, comprising rats i.p. injected with saline; chronic treatment, comprising rats receiving methylprednisolone in drinking water (6 mg/kg per day for 30 days); and chronic control, comprising rats receiving normal drinking water. Results: The levels of TRAP were significantly higher in the acute treatment group rats than in the acute control rats, suggesting an improvement in the pulmonary defenses of the former. The levels of lung LPO were significantly higher in the chronic treatment group rats than in the chronic control rats, indicating oxidative damage in the lung tissue of the former. Conclusions: Our results suggest that the acute use of corticosteroids is beneficial to lung tissue, whereas their chronic use is not. The chronic use of methylprednisolone appears to increase lung LPO levels.

Keywords: Lung; Methylprednisolone; Glucocorticoids; Lipid peroxidation; Antioxidant response elements.