Kennedy et al. (26) has done extensive studies on sudomotor innervation in human and experiment diabetic neuropathy. Most of the experimental studies were done on experimental diabetes in the mouse. They provided detailed ultrastructural studies of the mouse sweat gland (27). Many nerve fibers are entwined with the secretory tubule and contain accumulations of round, clear vesicles, some microtubules, but apparently no neurofilaments. Cholinesterase is found in the clefts between nerve fibers and their ensheathing Schwann cells. The nerve fibers tend to run parallel with capillaries, but have no close association with either the capillaries or the secretory epithelium. Capillaries provide an abundant blood supply to the sweat gland and are fenestrated. The relationships between cellular elements of the sweat gland provide no direct evidence of the mechanisms involved in neurogenic sweating, although it seems likely that effector substances are diffusely distributed. These workers described a reduction with aging, in sudomotor territories, the complement of sweat glands for individual nerves, the number of sweat glands responsive to cholinergic stimulation, as well as their capabilities for compensatory reinnervation of sweat glands by regeneration and by sprouting (28).
Cardone et al. (29), in a detailed and careful study of the sweat response in STZ-induced diabetes in the rat, reported decreased sweating that paralleled severity of hyperglycemia. The pilocarpine-induced sweat responses in the hind foot pads of groups of control and streptozocin diabetic rats, in good and in poor glycemic control and with a crossover design after 20 weeks of diabetes, were evaluated with the silicone mold sweat test to determine the number of sweat droplets per group of foot pads. The sweat response was dose dependent and reproducible, disappearing with denervation and reappearing with reinnervation. In the good glycemic controlled group, the sweat response was not different from that of the control group for up to 136 days. In the poor controlled group, the sweat response became reduced (p < 0.005) at 16 days and progressively worsened: 40% of baseline values at 14 weeks (p < 0.001). After restoring euglycemia in the poor control group, a normal sweat response occurred at 12 days. These results show that human neuropathic deficit, failure of sweating, can be prevented or ameliorated by good glycemic control.
Secretomotor functional impairment of parotid and submandibular glands has been reported in experimental diabetes. The right parotid ducts were cannulated and parotid salivary flow was induced by stimulating the sympathetic trunk in bursts (50 Hz, 1:10). Total protein and amylase output from the gland were reduced in diabetic animals compared with controls (30). A reduction in submandibular salivary protein concentration in response to sympathetic nerve stimulation was seen in rats that had been diabetic at 3 and 6 months (31). These changes were accompanied by a reduction in secretory granule release from acinar and granular duct cells.
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