Titov V N, Shiriaeva Iu K
Klin Lab Diagn. 2011 Apr(4):3-14.
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.
远端动脉床的微血管病变（MAP）发生在周细胞含量高且具有肌原纤维的结构中，这些周细胞通过与内皮细胞相互作用形成首批蠕动泵；它们将淋巴液、血淋巴和血液从动脉床推向静脉床。葡萄糖、高血糖、糖基化反应及其终产物在动脉床微血管间质组织损伤中的作用仅在围绕细胞间介质池的神经元轴突终末中有所体现，而其他轴突部分存在于不存在高血糖的脑脊液池中。当通过多元醇途径激活葡萄糖代谢时，内皮细胞质中会积累有机渗透溶质，如山梨醇，山梨醇会导致细胞过度水化，增加内皮细胞的高度。小动脉和毛细血管管腔变窄会增强外周血流阻力，导致灌注不足和慢性缺氧。此外，动静脉分流绕过交换毛细血管，使旁分泌群落中的细胞灌注不足和缺氧情况恶化，它将血液释放到静脉床中发挥作用。通过己糖胺途径激活葡萄糖代谢会产生糖毒素，如乙二醛和甲基乙二醛。作为双功能试剂，它们同时利用两端与蛋白质相互作用，在血管间质基质中的胶原纤维之间形成交联，不可逆地增强小动脉和毛细血管壁的硬度。随着壁硬度的增加，周细胞无法沿毛细血管推动血液流动，从而使灌注不足和缺氧情况恶化。在糖尿病中，高血糖持续存在且糖基化增加。血管壁中胶原蛋白结构向糖基化终产物的转化以及内皮生态生物学功能受损是间质组织炎症生物反应的一个原因。炎症生物反应的必然部分是活性氧的氧化作用以及丙二醛的产生，丙二醛也是一种双功能试剂。成纤维细胞增殖和动脉硬化是MAP的结果，MAP是小动脉和毛细血管壁中的一种破坏性炎症过程。
