Source: Annual Congress 2008 - Physiological response to exercise performance
Disease area: Airway diseases

Abstract

Rationale: recent studies have demonstrated that Angiotensin-Converting Enzyme inhibitor (ACEI) can improve peripheral skeletal muscle contractile function in patients with chronic heart failure (CHF). In light of the striking similarities in the etiology of myopathy between COPD and CHF, we hypothesized that ACEI may exert some beneficial effect on peripheral skeletal muscle of COPD. Methods: sixty-four SD rats were orotracheally instilled with 60 IU elastase (ESD) or saline solution (NSD). Twelve weeks later, sixteen rats from each group received water containing captopril (50mg/L) for 8 weeks. In situ mechanical properties of gastrocnemius were measured. Lipofuscin accumulation was evaluated as a marker of cellular oxidative damage. Immunohistochemistry was used for the detection of nitric oxide synthases (NOS). The activities of superoxide dismutase (SOD), catalase (CAT) and total antioxidant capacity (T-AOC) were measured in the muscle biopsy homogenate. Results: Captopril improved antifatigue tolerance, increased the proportion of type I fibers and decreased lipofuscin accumulation in gastrocnemius of ESD. Captopril enhanced the expression of endothelial NOS (eNOS), whereas exerted no effect on neuronal NOS (nNOS) or inducible NOS (iNOS) in gastrocnemius of ESD. In muscle homogenate, the activities of SOD, CAT and T-AOC were increased in ESD treated with captopril. Conclusions: ACEI may improve the antifatigue tolerance of peripheral skeletal muscle in emphysematous rats , which may be mediated by the shift of fiber type constitution, increase of antioxidant capacity , enhancement of eNOS expression and attenuation of oxidative damage.

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Citations should be made in the following way:
X. Zhang, C. Wang, B. Pang, J. Wang (Beijing, China). Effects of angiotensin-converting enzyme inhibitor on peripheral skeletal muscle dysfunction in emphysematous rats. Eur Respir J 2008; 32: Suppl. 52, 3300

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