Male wistar rats were made diabetic at 7 weeks of age by the injection of streptozotocin, 80mg/kg body weight. R-R interval variations (CV value) were recorded by electro-sphygmomanometer PE 300 with a recording speed of 1cm/second and measured light microscopically using a Nikon micrometer. CV values were 3.12±0.20% in diabetic rats at 6 weeks' duration of diabetes, which was significantly decreased compared with 4.12±0.34% in control rats (p<0.05), similar to autonomic neuropathy in human diabetics.
Atrial ganglion cells were studied pathologically with Kliiger-Barrela staining.: Ganglion cells of control rats showed clear nucleic membranes and nucleic bodies, and diffusely and finely disseminated Nissl bodies in cytoplasma, while diabetic rats showed lysis or picnosis of nuclei with peripherally located aggregated and in creared Nissl bodies. These findings were similar to those in celiac ganglion cells in human diabetics. These data suggest diabetic autonomic neuropathy (parasympathetic) might take place in diabetic rats.
Plasma catecholamine levels, determined by high-performance liquid chromatography, were elevated in response to blood withdrawal in normal rats. Such a response was also observed in streptozotocin diabetic rats 2 and 6 weeks after the onset of disease but was no longer seen at 13 weeks. Tissue (adrenal, heart, skin, kidney) catecholamine levels in diabetic rats were increased at 6 weeks as well as at 13 weeks. These abnormalities were corrected by insulin treatment in at least some of the diabetic rats. The present data suggest that there might be a catecholamine accumulation, which is later accompanied by impaired catecholamine secretion in diabetic rats, and they provide a basis for the inference that similar changes might play some role in the pathogenesis of diabetic autonomic neuropathy in humans.
