Titov V N, Shiriaeva Iu K
Klin Lab Diagn. 2011 Jul(7):3-14.
The microangiopathy under hyperglycemia and diabetes develops only in the microcirculation component of circulatory system. In this area considerable amount of pericytes is concentrated. These cells contain myofibrils and in circulatory mode envelop capillaries being situated on the outside of basilemma. It is possible that in a phylogenetic sense this is the earliest functional unity of endothelium monolayer as a pacemaker and pericytes as contractile elements which are the earliest "propeller" because of implementing the function of advancement of lymph, hemolymph and blood in capillaries. Probably, endothelium and pericytes formed the first variation of peristaltic "pump" for the purpose of blood advancement longwise of capillaries. Most probably, the state of distal part of arterial race (muscular type arterioles) impact the parameters of proximal part of arterial race (elastic type arterioles) and myocardium itself in the same extent as the state of "pump" in capillaries, endothelium and pericytes function impact the function of local peristaltic pumps (muscular type arterioles) in paracrine cenosis. It is supposed that the pericytes are the regulators of physical, hydraulic factor of activation of biologic reaction of transcitosis--excretion of nutrients and humoral mediators from capillaries to the pool of intercellular medium to perform the biologic function of homeostasis. Hyperglycemia, glycotoxins formation, bivalent substances (glyoxal, methilglyoxal, malonic dialdehyde) reacting simultaneously by both ends of molecule result in formation within collagen of areolar tissue of short transversal cross-links (glycosylation end product) which significantly increase rigidity (hardness) of capillary wall. In these conditions, myofibrils of pericytes no longer form directed deformation of capillary wall to effect peristalsis and advancement of hemolymph (blood later on) along capillaries according the synthesis of monolayer endothelium NO as a dilatation factor. This is the cause of blood circulation disturbance on the level of exchange capillaries and formation of chronic hypoxemia resulting in the only increase of rate of glycosylation chemical reaction. The microangiopathy is formed in the cells and tissues in an integrated pool of intercellular medium and never occurs in the cerebrospinal fluid pool where no hyperglycemia develops.
高血糖和糖尿病状态下的微血管病变仅发生在循环系统的微循环部分。在该区域集中了大量的周细胞。这些细胞含有肌原纤维，在循环过程中包绕位于基底膜外侧的毛细血管。从系统发育的角度来看，内皮单层作为起搏器，周细胞作为收缩元件，可能是最早的功能统一体，由于其实现了淋巴、血淋巴和血液在毛细血管中的推进功能，所以是最早的“推进器”。内皮和周细胞可能形成了第一种蠕动“泵”，用于沿毛细血管纵向推进血液。很可能，动脉段远端（肌型小动脉）的状态对动脉段近端（弹性型小动脉）和心肌本身参数的影响程度，与毛细血管中“泵”的状态、内皮和周细胞功能对旁分泌环境中局部蠕动泵（肌型小动脉）功能的影响程度相同。据推测，周细胞是转胞吞生物反应激活的物理、水力因素的调节者，即营养物质和体液介质从毛细血管向细胞间液池的排泄，以实现内环境稳态的生物学功能。高血糖、糖毒素形成、分子两端同时发生反应的二价物质（乙二醛、甲基乙二醛、丙二醛）导致在疏松结缔组织的胶原内形成短的横向交联（糖基化终产物），这显著增加了毛细血管壁的硬度。在这些情况下，周细胞的肌原纤维不再根据单层内皮合成的作为扩张因子的一氧化氮，形成毛细血管壁的定向变形以实现蠕动和血淋巴（后来的血液）沿毛细血管的推进。这就是交换毛细血管水平血液循环紊乱以及慢性低氧血症形成的原因，导致糖基化化学反应速率仅增加。微血管病变在细胞间液的综合池中形成于细胞和组织中，绝不会发生在不发生高血糖的脑脊液池中。
