Extrajunctional acetylcholine sensitivity of inactive muscle fibres in the baboon during prolonged nerve pressure block.

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Abstract
1. Nerve‐evoked muscular activity was abolished in the small hand muscles of the baboon for 1‐2 months by a 3 hr period of nerve compression from a pneumatic tourniquet inflated round the forearm. In the large diameter nerve fibres, this produced either a prolonged conduction block due to local myelin damage at the site of compression, or (in 10‐30% of the large fibres) Wallerian degeneration. 2. At varying intervals after nerve compression the extrajunctional acetylcholine (ACh)‐sensitivity of innervated but inactive muscle fibres in the fourth lumbrical muscle was measured. Observations were also made on lumbrical muscle fibres at similar intervals after surgical denervation. 3. The ACh sensitivity of nerve‐blocked muscle fibres started to develop later than in denervated muscle fibres (10 vs. 7 days) and remained at a lower level (40‐80 mV/nC, median ACh‐sensitivity) than that of denervated muscle fibres (200‐437 mV/nC) from 21 to 63 days after nerve block or denervation. 4. In stimulation experiments on four muscles, extrajunctional ACh‐sensitivity of both denervated and innervated but inactive fourth lumbrical muscle fibres was reduced by muscular activity. 5. In four animals mild compression was used in the lower limb to produce persistent nerve block without Wallerian degeneration. With one exception (in which some Wallerian degeneration had occurred) recording with a co‐axial needle from abductor hallucis showed no spontaneous fibrillation up to 28 days after compression, although the extrajunctional ACh‐sensitivity of the muscle fibres appeared to reach levels similar to those observed in the forelimb. All four muscles developed a slight increase in insertion activity after 1‐2 weeks. 6. It may be concluded that both muscular activity and some other neural influence, independent of muscular activity, are able to influence extrajunctional muscle properties in the baboon. The neural influence appears to be more effective in preventing spontaneous fibrillation than in preventing a rise in ACh sensitivity of the extrajunctional muscle membrane.