ISSN:
1573-6865
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Synopsis A histological and histochemical investigation was carried out of the changes in the anterior tibialis muscle of rats following double ligature and the severing of the common iliac artery on the right side during the acute and the chronic stage of ischaemia. In addition, the influence of physical conditioning over a period of 4 weeks on the ischaemic muscle was studied in two experiments; in the first, training started 2 weeks after ligature and in the second, 7 weeks after ligature. The most severe changes were found in the muscle after ischaemia had lasted for 7 days. They presented a typical form of necrosis and, histochemically, either very low or no succinate and malate dehydrogenase activity. The zone of tissue surrounding the necrotic focus showed morphological signs of regeneration; the histochemical signs, particularly succinate and malate dehydrogenase activity, manifested themselves later, i.e. after ischaemia had lasted for 4 weeks. Eleven weeks after ligature, the ischaemic muscle appeared morphologically regenerated, but on histochemical examination, it was found that the succinate and malate dehydrogenase activities were lower in the regenerated muscle fibres than in the controls. After physical conditioning, there was a tendency towards improvement of the metabolic condition of ischaemic muscle in the first series, while the activities of the dehydrogenase systems in the second series reached levels as high as those in the controls. Although the ischaemic muscle eventually regenerates spontaneously, slight physical conditioning assists in improving the metabolic condition of the affected muscle. However, it is important to determine the most suitable moment for the start of these exercises. The results of the experiments described indicate that improvement is better if training is started after the acute phase has subsided.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF01011803
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