Open AccessLight and Electron Microscopic Changes in Cardiac and Skeletal Muscle of Sheep with Experimental Monensin Toxicosis
Author(s) -
Anthony W. Confer,
D. U. Reavis,
Roger J. Panciera
Publication year - 1983
Publication title -
veterinary pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.794
H-Index - 89
eISSN - 1544-2217
pISSN - 0300-9858
DOI - 10.1177/030098588302000511
Subject(s) - monensin , myofibril , skeletal muscle , necrosis , creatine kinase , myopathy , cardiac muscle , endocrinology , edema , medicine , fibrosis , sarcoplasm , myocyte , pathology , biology , calcium , biochemistry
Monensin toxicosis was induced in lambs by either a single oral dose of 12 mg/kg or six daily doses of 8 mg/kg. Clinical signs of toxicosis consisted of depression, dyspnea, stiffness of gait, reluctance to move, and recumbency. Serum creatine phosphokinase activity was increased. Samples of skeletal and cardiac muscle were obtained over a six-day period and examined by light and electron microscopy. Light microscopic changes in cardiac and skeletal muscles consisted initially of vacuolation and intracellular edema of muscle cells followed by segmental necrosis. Interstitial fibrosis was present on days 5 and 6 postexposure. Muscle fiber necrosis was more severe in skeletal than cardiac muscles and most severe in sheep given 8 mg/kg of monensin daily. Macrophages were seen only in areas of severe necrosis. The earliest ultrastructural change was severe swelling of mitochondria. Secondary changes consisted of lipid accumulation and myofibrillar alterations. Myoblast proliferation was present as early as four days after initial exposure to monensin.