OBJECTIVE To histologically evaluate and compare features of myofibers within the elongated soft palate (ESP) of brachycephalic and mesocephalic dogs with those in the soft palate of healthy dogs and to assess whether denervation or muscular dystrophy is associated with soft palate elongation. SAMPLE Soft palate specimens from 24 dogs with ESPs (obtained during surgical intervention) and from 14 healthy Beagles (control group). PROCEDURES All the soft palate specimens underwent histologic examination to assess myofiber atrophy, hypertrophy, hyalinization, and regeneration. The degrees of atrophy and hypertrophy were quantified on the basis of the coefficient of variation and the number of myofibers with hyalinization and regeneration. The specimens also underwent immunohistochemical analysis with anti-neurofilament or anti-dystrophin antibody to confirm the distribution of peripheral nerve branches innervating the palatine myofibers and myofiber dystrophin expression, respectively. RESULTS Myofiber atrophy, hypertrophy, hyalinization, and regeneration were identified in almost all the ESP specimens. Degrees of atrophy and hypertrophy were significantly greater in the ESP specimens, compared with the control specimens. There were fewer palatine peripheral nerve branches in the ESP specimens than in the control specimens. Almost all the myofibers in the ESP and control specimens were dystrophin positive. CONCLUSIONS AND CLINICAL RELEVANCE These results suggested that palatine myopathy in dogs may be caused, at least in part, by denervation of the palatine muscles and not by Duchenne- or Becker-type muscular dystrophy. These soft palate changes may contribute to upper airway collapse and the progression of brachycephalic airway obstructive syndrome.

Skeletal muscles from healthy dogs and Labrador Retrievers with hereditary muscular dystrophy were examined morphologically and histochemically and were analyzed biochemically for Na+, K+, Ca2+, Mg2+, Zn2+, Cu2+, Cl-, total muscle water, and total neutral lipid content. Flame atomic absorption spectrophotometer was used for elemental quantitation of hydrochloric acid tissue extracts. Muscle samples from dystrophic dogs contained substantially increased concentrations of Na+, Ca2+, Zn2+, Cu2+, and Cl-, and a considerable reduction in the content of K+ and Mg2+ compared with samples from healthy dogs. Total muscle water and total fat content was higher in muscles from dystrophic dogs. Most muscle samples from dystrophic dogs had a type-2 fiber deficiency and an increase in number of fibers with internalized nuclei.

This study was carried out to determine the prognostic importance of troponin enzyme levels in lambs with White Muscle Disease (WMD). Materials and Methods: This study consisted of 50 male and female lambs aged 0-3 months old, 30 of which had clinical white muscle disease (Group I) and 20 of which were healthy (Group II – Control Group). Group I was composed of lambs that showed clinical symptoms of the disease. The disease was also identified by laboratory analysis. The lambs in this group were treated and the course of the disease was followed for 15 days.Compared with the control group, the Group I before treatment results were as follows: AST, LDH, CK, CK-MB, Troponin I and T (P<0.001) were high, while GSH-Px (P<0.001), SOD (P<0.01), Se (P<0.01), Retinol and Tocopherol were low. Compared with the control group, the Group I After Treatment results were as follows: AST, CK, Troponin T (P<0.001) were high, LDH (P<0.01) was high and GSH-Px (P<0.01) was low. Comparing Group I Before Treatment and After Treatment results, AST, CK, CK-MB and Troponin I (P<0.001), as well as GSH-Px, SOD and Se (P<0.01) were high. It was determined that LDH decreased and Tocopherol increased. Whereas Vitamin D3 was determined to be insignificant in all three groups, the levels of CK-MB, Troponin I, Retinol, SOD and Se were insignificant in the After Treatment and control groups, and the Troponin T and retinol values were measured to be insignificant in the Before Treatment and After Treatment groups.To conclude, measuring the AST, CK, CK-MB, LDH values as well as Troponin can be an important parameter for the identification and prognosis of WMD.

Explants were prepared from skeletal muscle tissue from 5 nondystrophic pups and from 5 pups with X-linked muscular dystrophy; pups were 2 to 17 weeks old. A serial reexplant method resulted in optimal cell density with minimal fibroblast growth. Cultures were examined daily by use of phase-contrast microscopy; differentiated (postfusion) cultures were examined by electron microscopy. Moderate nuclear pleomorphism and cell clustering were observed in cultures of normal and dystrophic muscle cells. Cultures were maintained to 27 days after plating. Minimal myofilament synthesis was observed in multinucleate cells from nondystrophic and dystrophic pups, but spontaneous contraction of myotubes was not observed during this period. Differences in growth, fusion, or differentiation of myogenic cells into multinucleate cells and myotubes were not found between dystrophic and normal muscle.

Clinical electromyographic studies were performed in dogs (6 weeks to 5.5 years old) with a degenerative myopathy analogous to Duchenne muscular dystrophy. Spontaneous activity, consisting primarily of complex repetitive discharges (pseudomyotonic discharges), was found in all dogs tested, but was most prominent in dogs greater than or equal to 10 weeks old. Myotonic discharges also were found, but were less frequent. Motor unit potentials were generally abnormally brief and frequently polyphasic. Ulnar nerve conduction velocities determined in two 4-month-old dogs were similar to those of unaffected littermates. It was concluded that canine X-linked muscular dystrophy is a primary myopathic process in which complex repetitive discharges and myotonic discharges are a prominent feature. The basis for this spontaneous activity is not known.