NEUROEFFECTOR CHARACTERISTICS OF SWEAT GLANDS IN THE HUMAN HAND ACTIVATED BY REGULAR NEURAL STIMULI

1. Intraneural electrical stimuli (0.3-1.2 mA, 0.2 ms) were delivered via a tungsten microelectrode inserted into a cutaneous fascicle in the median nerve at the wrist in twenty-eight normal subjects. The effects on sweat glands within the innervation zone were monitored as changes of skin resistance and water vapour partial pressure (WVPP). Regional anaesthesia of the brachial plexus in the axilla eliminated spontaneous sympathetic activity and reflex effects. 2. At stimulation frequencies of 0.1 Hz each stimulus evoked a transient skin resistance reduction, the amplitude of which varied initially but reached a steady state of less than 10 k-OMEGA after, on average, nine responses. If preceded by stimulation-free intervals of 5 min or more, up to fifteen stimuli were required before the first response occurred. With higher frequencies individual responses started to merge, skin resistance levels decreased successively and levelled off around 10 Hz. The total change of resistance (0-10 Hz) was 101 +/- 46 (n = 9) k-OMEGA and the higher the prestimulus level, the larger the reduction (r = 0.68, P < 0.05). 3. Stimulus-response latencies to the onset of a skin resistance reduction (single stimuli or trains of six impulses/20 Hz given at 0.1 Hz) shortened initially but reached steady-state values after on average nine to twelve impulses. Average conduction velocity between stimulating electrode and skin resistance recording site was 0.78 m/s and average time for electrical neuroeffector transfer in sweat glands was estimated to be 348 ms. 4. In addition to direct stimulation-induced resistance responses there were also small spontaneous reductions of resistance. They were seen in all subjects and at all frequencies but were more common in some subjects and occurred predominantly at the beginning of stimulation or at changes of frequency. They occurred independently at two skin sites in the same subject and disappeared during stimulation-free periods and after atropine. 5. With train stimulation (six impulses/20 Hz) at 0.1 Hz, each train evoked transient increases of WVPP of 1 mmHg or less in some subjects (latency around 1.6 s). After averaging weak increases were seen also after single stimuli in two subjects. Increases of stimulation current or frequency led to slowly developing sustained increases of WVPP concomitant with decreases in skin resistance. 6. Responses in skin resistance and WVPP to train stimulation at 0.1 Hz were suppressed in a dose-dependent way by I.V. injections of atropine. The cumulative dose necessary for complete inhibition of stimulus-induced responses (0.32 mg or less) had only weak effects on skin resistance responses to arousal stimuli in the opposite, non-anaesthetized hand. 7. We conclude that the intraneural electrical stimulation evoked sweating mainly by direct excitation of cholinergic sudomotor nerve fibres but that a minor addition of sweat was produced by a local mechanism in sweat glands and/or terminal nerve fibres. The delayed development of skin resistance responses after prolonged inactivity and the variability of stimulus-response latencies may indicate either that a certain degree of duct filling is required before skin resistance responses can be measured and/or that the mechanism for sweat production needs potentiation before becoming effective.