[A biochemical study of an animal model with defective muscle glycolysis, induced by iodoacetate administration].

A rat model produced by intraaortic injection of sodium iodoacetate was analyzed biochemically. Hind leg muscles obtained from iodoacetate-injected site showed a selective inhibition of the glyceraldehyde-3-phosphate dehydrogenase (G3PD) activity less than 10% of control mean. No loss of mitochondrial enzyme activity was observed. Electrical stimulation at the sciatic nerve revealed muscle contractures and this muscle showed a mild degeneration in histochemically. This study indicates that this model will be useful to study the pathophysiology of human muscle glycogen storage diseases.