Showing papers on "White Muscle Disease published in 2011"

Evaluation of the levels of homocysteine, troponin I, and nitric oxide in lambs with subclinical white muscle disease

Abstract: Summary White muscle disease (WMD) or Nutritional myodegeneration disease (NMD) is a degenerative disease of the cardiac and skeletal muscles. The level of serum activity of Plasma homocysteine (Hcy), cardiac troponin I (cTn I), Nitric oxide (NO) were investigated in lambs with subclinical NMD in this study. Ten healthy lambs and twenty lambs with subclinical NMD were used in this study. The blood samples were firstly taken at the onset of the disease and then 3 and 10 days after treatment in NMD, and taken once control group. The values of serum activity of creatin kinase (CK), aspartate aminotranferase (AST), alanine aminotranferase (ALT), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were measured with autoanalyzer. Plasma concentration of Hcy, serum cTn I, and levels of NO were determined with ELISA method and value of activity erythrocyte glutathione peroxidase (GSH-Px) was measured with spectrophotometer. Before treatment, values of plasma Hcy, serum NO, cTn I, AST, ALT, ALP, CK, and LDH in lambs with NMD were higher than those of healthy ones (P<0.001), while GSH-Px activity of lambs with NMD are lower than those of healthy (P<0.001). After ten days of treatment, there were no significant diff erences between treated lambs with NMD and healthy lambs. Nutritional myodegeneration in lambs is associated with increased levels of Hcy, cTn I, and NO. Increased levels of Hcy, cTn I, and NO may be a result of selenium deficiency causing myocardial disorder in NMD lambs.

Aspectos morfológicos de biópsias musculares em equinos com miopatia sob forma de surto

Abstract: Equine myopathies are classified according clinic, morphologic and molecular features in three groups: Non-exertional, exertional, and abnormal muscle membrane conduction. In spite the advances in diagnostic, the literature has reported outbreaks of equine myopathy without clear etiology in several countries. The aim of this study was to describe the histological and histochemical findings of muscle biopsies in an outbreak of equine myopathy. Seven 18 to 24-month-old Quarter horses showed clinical signs of myopathy. Five horses presented mild clinical signs and two horses had severe clinical signs with recumbency. Muscle biopsies were obtained from gluteal medium muscle by percutaneous technique with Bergstrom needle in all affected horses. Muscle samples were processed by histological (HE, modified gomori-trichrome) and histochemical (PAS, NADH, ATPase) technics. In animals with mild clinical signs, ragged red fibers type I and IIA, related to the oxidative metabolism dysfunction of mitochondria, was the main abnormality found. Muscle fiber atrophy and presence of subsarcolemmal aggregates in type I and IIA muscle fibers were also observed. More severe affected horses presented inflammatory infiltrate, proliferation of collagen, phagocytosis, necrosis and calcification. Based on the morphological findings, vitamin E therapy response associated with the low mortality when compared with atypical myopathy reports, We concluded that this outbreak was triggering for mitochondrial lesions, characterized by ragged red muscle fibers, probably due a breakdown homeostasis in vitamin E and Se, being compatible with nutritional myopathy diagnosis.