糖尿病患者的靶器官处于动脉僵硬和微循环损伤之间。

Achille Cesare Pessina
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引用次数: 18

摘要

高血压和糖尿病经常同时发生。文献中有一个普遍的共识,即高血压和糖尿病患者的心脏和肾脏被锁在一个陷阱中,在动脉硬化和微循环损伤之间,每种情况都在恶性循环中相互促进。葡萄糖耐量降低与大血管厚度和硬度增加有关,从而导致血压升高、大血管并发症和肾功能受损。大动脉僵硬导致微血管损伤,进而增加毛细血管稀疏(最初由高血压和糖尿病引起)和波反射。收缩压和脉压随之升高,导致循环结束,微血管损伤加重。此外,大血管和微血管损伤似乎会使血压升高,损害靶器官的组织灌注,高血压患者外周血微血管的血管结构改变与冠状动脉血管扩张剂能力受损有关。这些机制得到了大量研究数据的支持,这些研究调查了糖尿病和高血压对微血管形态和功能的影响,其中一些似乎发生在糖代谢受损,在发展为全面糖尿病之前。这些变化也具有重要的预后价值,冠状动脉血管收缩与心血管事件的发生率直接相关。打破事件循环的干预措施是可用的,含有血管紧张素转换酶抑制剂的方案在增加冠状动脉储备方面显示出良好的疗效。一些机制似乎集中在抑制缓激肽降解,而不是对肾素-血管紧张素-醛固酮系统的影响。
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Target organs of individuals with diabetes caught between arterial stiffness and damage to the microcirculation.

Hypertension and diabetes mellitus occur together frequently. There is general consensus in the literature that in patients with hypertension and diabetes, the heart and kidneys are locked in a vice, between arterial stiffening and damage to the microcirculation, with each condition feeding the other in a vicious cycle of events. Decreased glucose tolerance is associated with increased thickness and stiffness of large blood vessels, which contributes to increased blood pressure, macrovascular complications and impaired renal function. Large artery stiffness causes damage to the microvasculature, which in turn increases both capillary rarefaction, initially generated by hypertension and diabetes, and wave reflection. Systolic and pulse pressure are consequently increased, which results in completion of the cycle with more microvascular damage. In addition, macro and microvascular damage appears to increase blood pressure and impair tissue perfusion to target organs, and alterations to the vascular structure of peripheral microvessels in hypertension are related to the impairment of coronary vasodilator capacity. These mechanisms are supported by a large body of data from studies investigating the effects of diabetes and hypertension on the morphology and function of the microvasculature, some of which appear to occur in impaired glucose metabolism, preceding the development of full-blown diabetes. These changes also have important prognostic value, with direct correlations between coronary artery vasoconstriction and the incidence of cardiovascular events. Interventions to break the cycle of events are available, and regimens containing angiotensin-converting enzyme inhibitors have demonstrated good efficacy in increasing coronary reserve. Some of the mechanisms appear to be centred around the inhibition of bradykinin degradation rather than an effect on the renin-angiotensin-aldosterone system.

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