Arosio E, Minuz P, Prior M
Cattedra di Terapia Medica, Università degli Studi di Verona.
Ann Ital Med Int. 1999 Apr-Jun;14(2):106-13.
The role of endothelial dysfunction in the pathogenesis of diabetic microangiopathy is reviewed. Reversible alterations in microcirculation, consisting of increased capillary pressure, blood flow and endothelial permeability, can be detected at an early stage in diabetes mellitus. Irreversible structural modifications of the vascular wall, such as thickening of the basal membrane due to the extracellular accumulation of proteins, take place at later stages. Atherosclerosis further affects microcirculation in diabetes mellitus by decreasing autoregulatory capacity and blood flow reserve. Endothelial dysfunction has been observed to precede the onset of microvascular lesions, as demonstrated by reduction in the vasodilatory response to vasoactive agents and by alterations in the antithrombotic properties of the endothelium. Experimental data available so far suggest that endothelial dysfunction may be directly related to hyperglycemia. Abnormalities in lipoprotein metabolism, generation of glycation end products, and increased oxidative stress may also be responsible for the endothelial dysfunction in diabetes mellitus. Insulin resistance appears to be related to endothelial dysfunction in non-insulin-dependent diabetes mellitus through a reduction in the biological activity of endothelial-derived nitric oxide.
本文综述了内皮功能障碍在糖尿病微血管病变发病机制中的作用。在糖尿病早期即可检测到微循环的可逆性改变,包括毛细血管压力、血流量和内皮通透性增加。后期会发生血管壁的不可逆结构改变,如由于蛋白质在细胞外积聚导致基底膜增厚。动脉粥样硬化通过降低自动调节能力和血流储备进一步影响糖尿病患者的微循环。内皮功能障碍已被观察到先于微血管病变的发生,这表现为对血管活性药物的血管舒张反应降低以及内皮抗血栓特性的改变。目前可得的实验数据表明,内皮功能障碍可能与高血糖直接相关。脂蛋白代谢异常、糖基化终产物的生成以及氧化应激增加也可能是糖尿病内皮功能障碍的原因。在非胰岛素依赖型糖尿病中,胰岛素抵抗似乎通过降低内皮源性一氧化氮的生物活性与内皮功能障碍相关。