Histochemical and ultrastructural study of human muscles after spontaneous rupture of the tendon.
The authors studied the histochemical and ultrastructural alterations of human muscles after spontaneous rupture of the tendon. Both succinate dehydrogenase (in type 1 fibres), and ATPase (in type 2 fibres) activity decreased in all injured muscles. In the intact antagonists and in contralateral muscles alterations were not found. The creatine phosphokinase and aldolase activity were decreased also in the injured muscles. The lactate dehydrogenase activity was various both in affected and in unaffected antagonists muscles. 2 weeks or more after the rupture of the tendon, in the injured muscles the number of type 1 fibres were decreased and therefore a statistically significant type 2 fibre predominance occurred. Ultrastructurally the disruption and disorientation of the myofibrils, streaming and disorganisation of Z line were found. The sarcolemma was arranged, the sarcoplasmic reticulum was dilated; both normal, pycnotic and enlarged mitochondria were observed. The motor end-plates were not discernible.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000328:Adult; D003402:Creatine Kinase / Q000378:metabolism; D005260:Female; D005634:Fructose-Bisphosphate Aldolase / Q000378:metabolism; D006801:Humans; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009132:Muscles / Q000201:enzymology / Q000473:pathology* / Q000648:ultrastructure; D009210:Myofibrils / Q000648:ultrastructure; D006005:Phosphorylases / Q000378:metabolism; D012422:Rupture, Spontaneous; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013708:Tendon Injuries / Q000473:pathology*
D007770:L-Lactate Dehydrogenase; D013385:Succinate Dehydrogenase; D006005:Phosphorylases; D003402:Creatine Kinase; D000251:Adenosine Triphosphatases; D005634:Fructose-Bisphosphate Aldolase