We have quantified postganglionic sweat output in human subjects resulting from axon reflex stimulation using acetylcholine electrophoresis. Dehumidified nitrogen of controlled temperature and flow rate was passed through an acrylic plastic chamber placed over a defined area of skin. Sweat droplets were evaporated; humidity change was sensed by a narrow-range humidity sensor housed in a temperature-controlled compartment and was plotted on a chart recorder. The time integral (area under the curve) was continuously integrated and converted to absolute units using a derived equation. Because stimulation and recording were simultaneous, an accurate determination of the latency of the sweat response was also possible. Quantitative sudomotor axon reflex tests were performed on the left forearm and foot of 33 female and 29 male normal subjects aged 11 to 69 years. Acetylcholine, 10%, was electrophoresed for 5 mA-minutes in the forearm and 10 mA-minutes in the foot, and recording was continued for an additional 5 minutes. The mean sweat output in males was 2.7 and 3.0 times that in females in forearm and foot, respectively (p less than 0.0001). Studies in selected autonomic neuropathies confirm that quantitative sudomotor axon reflex tests will detect postganglionic sudomotor abnormalities sensitively and reproducibly.

Endoneurial hypoxia has been postulated to be important in the pathogenesis of diabetic peripheral neuropathy and may be due to reduced nerve blood flow. Neither blood flow nor oxygen tension have previously been measured in peripheral nerve in diabetic neuropathy. We have therefore measured both nerve blood flow and endoneurial oxygen tension in the sciatic nerves of 8 rats with streptozotocin-induced diabetes for four months, and in 8 age-matched controls. In 7 of the diabetic animals mean nerve blood flow was 8.7 +/- 1.3 ml X min-1 X 100 g-1 which is significantly less than mean nerve blood flow in the controls (13.08 +/- 0.8 ml X min-1 X 100 g-1; P less than 0.01). In one diabetic animal, nerve blood flow was too low to be accurately measured. The reduction in nerve blood flow in diabetic neuropathy is due to an increase in resistance to flow which may be due to microangiopathy and to blood hyperviscosity. Endoneurial oxygen tension was also significantly reduced in experimental diabetic neuropathy in which 60 per cent of the oxygen measurements were less than 25 mmHg, compared with 19 per cent in the controls. Nerve blood flow was also measured in rats with experimental galactose neuropathy in which there is more marked sugar-alcohol accumulation, endoneurial oedema and elevation of endoneurial fluid pressure than in experimental diabetic neuropathy. The results obtained in this neuropathy suggest that the reduction in nerve blood flow which occurs in experimental diabetic neuropathy is due largely to factors other than sugar-alcohol accumulation in nerve. We postulate that endoneurial hypoxia may produce many of the observed morphological and biochemical changes in experimental diabetic neuropathy.

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