Contribution of circulating acetylcholine to sensory nerve conduction augmentation

We previously discovered that sensory nerve action potential amplitudes inc reased during isometric muscle contraction and that this response could be blocked with tourniquet isolation of the contraction source. The hypothesis far this study was that a circulating factor was responsible for this effe ct. In this prospective study, baseline and post intravenous injection of s erial sural nerve action potential recordings were made in the leg of 8 rab bits. The sequence of the injections was randomized: 1) normal saline place bo, 2) 0.01 mg/kg acetylcholine (ACh) 3) 200 mg/kg Na acetate, 4) 260 mg/kg Na lactate, and 5) 20 mg/kg choline. Results showed there was a 3.8 mu V i ncrease in the sural nerve response 6 min after ACh injection compared to b aseline at rest (p = .01, power = .9, analysis of variance (ANOVA), repeate d measures). There were no significant changes in the amplitudes of the sur al nerve after injection of the remaining agents or placebo (p = .33 to .81 , ANOVA, repeated measures). In conclusion, circulating ACh is the only age nt tested thus far that appears to be responsible for this effect. In addit ion, the amplitude and temporal curve of this response is similar to that s een after exercise in human subjects. The clinical importance of this study is that ACh plays a role in this newly discovered sensory regulatory mecha nism controlled by the motor system.