Sakharnyy diabet i endotelial'naya disfunktsiya

Yarek-Martynova, Ivona Renata; Shestakova, Marina V.

doi:10.14341/2072-0351-5609

Cited by 6 publications

(1 citation statement)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Such chronology of these changes is explained by the fact that hyperglycemia in different periods of the DM development activates different pathophysiological mechanisms. During the initial stages, moderate hyperglycemia stimulates the secretion of vasodilator mediators, among which the major one is nitric oxide, by the arterioles' endothelium [15], but chronic high hyperglycemiainhibits the synthesis of vasodilators [15,22]. The extension of arterioles and small arteries during the last two terms of the experiment is associated with impaired vasoconstrictive sympathetic innervation of vessels [3].…”

Section: Resultsmentioning

confidence: 99%

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

Tokaruk

2019

Galician med. j.

View full text Add to dashboard Cite

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.

show abstract

Section: Resultsmentioning

confidence: 99%

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

Tokaruk

2019

Galician med. j.

View full text Add to dashboard Cite

show abstract

The Role of Endothelium in the Regulation of the Aggregate State of Blood Under Normal Conditions, in Atherosclerosis and Arterial Hypertension

Makogonenko¹,

Gornytska²,

Gudzenko³

et al. 2021

Fiziol Zh

View full text Add to dashboard Cite

The structure and functions of the endothelium under normal conditions and a number of pathologies are reviewed in this work with the focus on its role in maintaining the balance between pro- and anticoagulant function of blood in different vascular beds. The role of endothelium in the synthesis and secretion of NO and other vascular regulators is highlighted. The mechanisms of its dysfunction, the role and interconnection of pathological changes in diseases such as atherosclerosis and hypertension are described.

show abstract

A new early diagnostic criterion for endothelial dysfunction in men

et al. 2017

View full text Add to dashboard Cite

Endothelial dysfunction (ED) triggers vascular complications in many diseases, including diabetes mellitus. Currently existing methods for detection of ED do not ensure early diagnostics of the pathological process. We examined 168 men with type 2 diabetes mellitus. ED was studied by ultrasound assessment of arterial vasoreactivity of the brachial artery and determination of biochemical ED markers. Based on manifestations of reactive hyperemia, the patients were divided into groups according to the presence or absence of ED. It was shown that 23.2%of the patients exhibiting normal endothelium-dependent vasodilation in response to the reactive hyperemia test had s.582 + 353_379del polymorphism of the endothelial nitric oxide synthase gene. We also demonstrated that the time till maximum vasodilatation in these patients was 33.3% longer, on the average, than in men who did not have such polymorphism. The slowdown of the maximum response of endothelium-dependent vasodilation was associated with increased levels of ED proteomic markers VCAM-1 and ICAM-1 in 27% and 22.9% of the cases respectively. Thus, we showed for the first time that the time till maximum vasodilation is a more reliable marker of ED than the difference between the diameters of the brachial artery during reactive hyperemia test expressed in percentage.

show abstract

Sakharnyy diabet i endotelial'naya disfunktsiya

Cited by 6 publications

References 41 publications

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

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

The Role of Endothelium in the Regulation of the Aggregate State of Blood Under Normal Conditions, in Atherosclerosis and Arterial Hypertension

A new early diagnostic criterion for endothelial dysfunction in men

Contact Info

Product

Resources

About