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  • Title: [Arteriolosclerosis and atherosclerosis. Pathology of the distal and proximal arterial bed. Pathogenesis of diabetic microangiopathy].
    Author: Titov VN, Shiriaeva IuK.
    Journal: Klin Lab Diagn; 2011 Apr; (4):3-14. PubMed ID: 21739639.
    Abstract:
    Microangiopathy (MAP) in the distal arterial bed develops in the structures high in pericytes that have myofibrils and, by interacting with the endothelium, form the first peristaltic pumps; they push lymph, hemolymph and blood from the arterial bed to the venous one. The role of glucose, hyperglycemia, a glycation reaction and its end products in microvascular interstitial tissue damage in the arterial bed is shown only in the neuron axon terminals that surround the pool of the intercellular medium while the other axonal parts are present in the cerebrospinal fluid pool where hyperglycemia is absent. When glucose metabolism is activated through the poliolovic pathway, the endothelial cytosole accumulates organic osmolytes, such as sorbitol alcohol that, by causing hyperhydration, increases the height of endothelial cells. The decreased lumen of arterioles and capillaries enhances peripheral resistance to blood flow to give rise hypoperfusion and chronic hypoxia. Moreover, by bypassing the exchange capillaries and worsening cellular hypoperfusion and hypoxia in the paracrine communities, the arteriolo-venular shunt that releases blood into the venous bed functions, by getting around the exchange capillaries. Glucose metabolism activation through the hexosamine pathway generates glycotoxins, such as glyoxal and methylglyoxal. As bifunctional reagents, they interact with proteins simultaneously, by using both ends, form cross-links between the collagen fibers in the vascular interstitial matrix and irreversibly enhance the rigidity of arteriolar and capillary walls. As the rigidity of the walls is increased, the pericytes are unable to move blood along the capillaries, by worsening hypoperfusion and hypoxia. In diabetes, hyperglycemia becomes persistent and glycation increased. The conversion of collagen structured in the vascular wall to glycosylation end products and the impaired biological function of endoecology are a cause of a biological reaction of interstitial tissue inflammation. The obligate part of the biological reaction of inflammation is the oxidation by reactive oxygen species and the generation of malondialdehyde, that is also a bifunctional reagent. Fibroblast proliferation and arteriosclerosis are a result of MAP as a destructive inflammatory process in the arteriolar and capillary walls.
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