Substantiation of the Results of Morphological Examination of the Urinary Bladder Wall in Experimental Diabetic Cystopathy

Measurement of consumed water and daily diuresis proved the pathomorphological manifestations of streptozotocin-induced -induced cystopathy in the experiment on rats according to the results of biochemical studies of blood and urine. It is argued that the desquamation of cells in the transitional epithelium, its atrophy, stratification violation, and baring of the basal membrane are caused by a large volume of urine, which excessively stretches the urinary bladder, destroying the intercellular contacts of the urothelial layer. It is proved that primary hyperglycemia leads to widening of the lumen of the arterioles and moderate thickening of the basal membrane of the micro-hemovessels, and high chronic hyperglycemia – directly triggers the whole cascade of pathomorphological changes: on the 42nd day of the experiment it causes vasoconstriction of the arterioles, and at the later terms – the secondary expansion of the arterioles and venules of the microcirculatory bed of UB (urinary bladder); is the cause of dystrophic changes of endothelial cells, further thickening and lamellar transformation of the basal membrane and plasma permeation of the perivascular connective tissue; causes the appearance of dark involutional myocytes with few organelles and sarcoplasm sequestration. Hydropic dystrophy of smooth myocytes has been found to be associated with the hydration of blood plasma as a result of excessive polydipsia in diabetic animals, and vacuole dystrophy of urothelial cells, enlargement of their size and interstitial edema – with low specific urinary density due to the multiple fast increase of diuresis. It has been established that prolonged high glucosuria and decreased diuresis lead to a decrease in urothelial cell size, compaction of their cytoplasm and ultrastructural readjustment. The increase of the content of glycosylated hemoglobin during the experiment justified the appearance and increase of the sludge-syndrome.