Energetic metabolism and fatigability in experimental myotonia.
Experimental myotonia was induced in rats by 2,4-dichloro-phenoxyacetic acid (2,4-D). After 4 to 24 h of treatment, the anterior tibialis muscles exhibited increased fatigue at low frequency (30 Hz) nerve stimulation, but they developed normal tension at high-frequency (100 Hz) stimulation. Glycogen content and the activities of glycogen phosphorylase, lactate dehydrogenase and malate dehydrogenase remained normal. The absence of correlation between fatigability and energetic metabolism in this experimental model of myotonia suggests a dysfunction in excitation-contraction coupling.
Ramírez
B U
BU
Departamento de Enfermedades Respiratorias, Pontificia Universidad Católica de Chile, Santiago.
D015084:2,4-Dichlorophenoxyacetic Acid; D000818:Animals; D004195:Disease Models, Animal; D004576:Electromyography; D004734:Energy Metabolism; D007274:Injections, Intraperitoneal; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008291:Malate Dehydrogenase / Q000378:metabolism; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects*; D009222:Myotonia / Q000139:chemically induced / Q000378:metabolism*; D006005:Phosphorylases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013268:Stimulation, Chemical; D013997:Time Factors
D015084:2,4-Dichlorophenoxyacetic Acid; D007770:L-Lactate Dehydrogenase; D008291:Malate Dehydrogenase; D006005:Phosphorylases