Abstract
Purpose: Recovery of muscle function after nerve repair remains incomplete despite progress in microsurgical techniques. Potential for muscle recovery could be greatly improved. The purpose of our study was to demonstrate the functional impact of exogenous satellite cells in degenerated muscles.
Material and methods: We used the anterior tibialis muscle (Ta) in rabbits (n=24) as our experimental model. Muscle degeneration was created by bilateral injections of cardio-toxin into the Ta. Five days later, the left Ta was injected with autologous satellite cells (SC) at multiple points. The same volume of culture medium was injected into the right Ta. Two months later, maximal isometric muscle force and stress resistance of the Ta was measured. Histoimmuno-chemical labellings were made.
Results: The volume of cardiotoxin injected created two categories of muscles: recovery of former function was not possible with low dose cardiotoxin injections. Maximal isometric muscle force was less than 35% of the control. Transfer of SC restored nearly normal muscle force. Resistance to stress followed the same pattern. Recovery of maximal muscle force was possible with high-dose cardiotoxin injections. Resistance to stress was greater than the control (+ 35%). Transfer of SC did not modify results.
The weight of the Ta increased for both cardiotoxin doses. There was an increase in the size of the fibres with or without SC transfer.
Discussion: Injection of cardiotoxin induced muscle degeneration. With greater muscle degeneration, regeneration of muscle capacity was greater. Transfer of SC improved the functional result when muscle degeneration was incomplete. Improved resistance to stress after injection of high-dose cardiotoxin could result from changes in muscle myosin and fibrillary structure.
Conclusion: Further studies are needed before clinical application to better understand the underlying mechanisms operating with satellite cell injections. Many applications could be proposed, particularly for surgical nerve repair, ischaemic heart failure, and myopathy.
The abstracts were prepared by Pr. Jean-Pierre Courpied (General Secretary). Correspondence should be addressed to him at SOFCOT, 56 rue Boissonade, 75014 Paris, France