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Peripheral nerve autografts increase soleus muscle hydrolase activity
Canadian Journal of Physiology and Pharmacology
|January 1, 1982
Summary
Nerve grafts on muscles trigger an inflammatory response, increasing specific enzymes and causing muscle damage. Protease inhibitors blocked this enzyme increase, suggesting inflammation is key to nerve-induced muscle degeneration.
Area of Science:
- Neuroscience
- Muscle physiology
- Enzymology
Background:
- Peripheral nerve autografts on muscles can cause acetylcholine hypersensitivity and myofibrillar damage.
- The underlying mechanisms of this muscle degeneration are not fully understood.
Purpose of the Study:
- To investigate the activity of acid protease, alkaline protease, and N-acetylglucosaminidase in rat soleus muscle after nerve transplantation.
- To evaluate the effect of protease inhibitors on these enzyme activities.
Main Methods:
- Rat soleus muscles were subjected to peripheral nerve autografts.
- Enzyme activity assays for acid protease, alkaline protease, and N-acetylglucosaminidase were performed.
- The impact of protease inhibitors (leupeptin and pepstatin) was assessed.
Main Results:
- A significant increase in acid protease, alkaline protease, and N-acetylglucosaminidase activity was observed three days post-nerve transplant.
- Leupeptin and pepstatin completely inhibited the nerve-induced elevation of hydrolase activity.
Conclusions:
- Muscle degeneration following nerve grafting appears to be a consequence of an inflammatory response initiated by the nerve.
- Protease activity is implicated in the pathogenesis of nerve-induced muscle injury.