role of sodium ions in the pathogenesis of skeletal muscle damage in broiler chickens

• Published in: Poultry science 2004-04, Vol.83 (4), p.701-706
• Main Authors: Sandercock, D.A, Mitchell, M.A
• Format: Article
• Language: English
• Subjects: adenosinetriphosphatase; Animals; Biological Availability; broiler chickens; calcium; Calcium - metabolism; Calcium Radioisotopes; cations; Chickens; creatine kinase; enzyme inhibitors; Female; in vitro studies; ion transport; monensin; Monensin - pharmacology; muscle tissues; Muscle, Skeletal - drug effects; Muscle, Skeletal - pathology; muscular diseases; Muscular Diseases - chemically induced; Muscular Diseases - veterinary; Ouabain - pharmacology; Poultry Diseases - chemically induced; skeletal muscle; sodium; Sodium - adverse effects; Sodium-Potassium-Exchanging ATPase - antagonists & inhibitors
• ISSN: 0032-5791; 1525-3171
• DOI: 10.1093/ps/83.4.701

The effect of sodium ions (Na+) on calcium (Ca2+)-mediated muscle damage in broiler chickens was investigated using an in vitro muscle preparation. Muscle Ca2+ accumulation was determined by 45Ca2+ uptake. Muscle damage was assessed by measurement of the efflux of the intracellular enzyme creatine kinase (CK) into the incubation medium. Loading muscle cells with Na+ by means of the sodium ionophore monensin led to concentration-dependent (25 to 200 micromolar) increases in 45Ca2+ uptakes and corresponding and proportional CK losses. The greatest responses occurred at 100 micromolar ionophore or greater, reflected in a 49% increase (P < 0.05) in 45Ca2+ uptake and an associated 140%-fold increase (P < 0.001) in CK efflux. Inhibition of muscle Na+/K+-ATPase activity with ouabain (2 mM) induced a 56% increase in 45Ca2+ uptake and a 60%-fold increase (P < 0.001) in total CK loss. The combined use of ionophore and ouabain resulted in 90 and 130%-fold elevations in 45Ca2+ uptake and CK loss, respectively. In monensin-treated muscles, inhibition of external Ca2+ influx from the incubation medium by chelation with 1,2 bis(2-aminophenoxy)ethane-N,N,N',N' tetracetic acid (5 mM) markedly reduced 45Ca2+ uptake (38%: P < 0.05) but increased CK release by 85% (P < 0.001). The results demonstrate that initial elevations in muscle Na+ can facilitate increases in muscle Ca2+ and lead to alterations in muscle cell membrane integrity and CK loss. The Na+-induced increases in myocellular Ca2+ may be mediated via direct extracellular Ca2+ entry or redistribution from internal Ca2+ stores. It is proposed that in order to reduce or prevent myopathies in poultry, exposure to conditions that may lead to elevations in muscle Na+ (e.g., increased muscle activity and stress or accidental ionophore toxicosis) should be avoided. The findings of this study have implications for management strategies of bird welfare, muscle pathology, and product quality.