Laboratory investigation; a journal of technical methods and pathology · 1986
Varied effects of experimental diabetes on the autonomic nervous system of the rat.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Kniel P C, Junker U, Perrin I V, Bestetti G E, Rossi G L
Аннотация
Disorders of the autonomic nervous system are a frequent late complication of human diabetes. They have been extensively studied clinically, yet their pathologic aspects are still poorly understood. Also, reports on the autonomic nervous system in animal models for diabetes are scanty. Therefore we have investigated sympathetic preganglionic and postganglionic nerve fibers, vagal fibers, as well as sympathetic and enteric neurons of male Wistar rats 1 year after streptozotocin or vehicle injection. By light and electron microscopic morphology we observed: various degenerative changes in sympathetic neurons and in Schwann cells of the sympathetic fibers; intraaxonal glycogen deposits in all fiber types; and a large amount of lipoid material in intraganglionic and endoneural mesenchymal cells. By morphometry, the cytoplasmic area and perimeter as well as the cytoplasmic to nuclear ratio were significantly reduced in the sympathetic neurons of diabetic rats. Further we found axonal dwindling, enlarged myelin-axons space and an increased number of Schwann cell pi-granules in the sympathetic preganglionic fibers of diabetic animals. Axonal glycogenosomes were absent in the vagus of control and were present in that of diabetic rats. By stereology, the mitochondria and smooth endoplasmic reticulum were reduced in the sympathetic neurons of diabetic rats, whereas in the same animals the volume density of the Golgi complex was increased in the sympathetic neurons and decreased in the enteric neurons. In conclusion, relevant changes occur in the sympathetic preganglionic nerve fibers which suggest a causal relationship between fiber and neuronal lesions. Further, the stereologic findings imply decreased cellular activity and imbalance between cellular synthesis and secretion in the sympathetic neurons.