Relationship between the Myopathy of 2,4-D and Other Experimental Myopathies. Formal Pathogenetic Relationship to Muscular Dystrophy in Man
The present study has established the principal symptoms of the myopathy of 2,4-D as predilective involvement of white (2B/Am) muscle fibres, occurrence of the earliest morphological changes in the mitochondria and the sarcoplasmic reticulum, loss of glycogen and phosphorylase activity closely related to the outcome of histological fibre damage and, finally, the sparing of the myocardium. Additional effects of this agent were found to be myotonia of skeletal muscle at early stages of intoxication (43, 268, 282), decelerated uptake of calcium by the vesicles of the sarcoplasmic reticulum (184) and, electrophysiologically, repetitive myotonic discharges (104, 268) due to the electrical hyperexcitability of the muscle fibre membrane. The pathogenetic relationship between myotonia and myopathy of 2,4-D origin is still unknown. If we compare the findings of the various experimental myopathies, it becomes evident that a close pathogenetic relationship exists between, on the one hand, the myopathy of 2,4-D and, on the other, muscular dystrophy of the mouse, myopathy of vincristine and myopathy of corticosteroids. This is particularly true of the initial proliferation of the mitochondria (49, 232, 296) and the decrease in phosphorylase activity and glycogen content of white muscle fibres in the early stages of the disease processes. The latter changes are paralleled by findings in the progressive muscular dystrophy of man (67, 115). Finally, in the experimental myopathies cited above, no involvement of the heart was observed.
KeywordsLactate Corticosteroid Immobilization Cardiomyopathy Myopathy
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