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急性交感神经阻断改善肥胖成人前臂胰岛素介导的微血管血流。

Acute Sympathetic Blockade Improves Insulin-Mediated Microvascular Blood Flow in the Forearm of Adult Human Subjects With Obesity.

机构信息

Division of Clinical Pharmacology, Department of Medicine Vanderbilt University Medical Center Nashville TN.

Division of Cardiology Vanderbilt University Medical Center Nashville TN.

出版信息

J Am Heart Assoc. 2024 Aug 20;13(16):e030775. doi: 10.1161/JAHA.123.030775. Epub 2024 Aug 9.

Abstract

BACKGROUND

Obesity is associated with resistance to the metabolic (glucose uptake) and vascular (nitric-oxide mediated dilation and microvascular recruitment) actions of insulin. These vascular effects contribute to insulin sensitivity by increasing tissue delivery of glucose. Studies by us and others suggest that sympathetic activation contributes to insulin resistance to glucose uptake. Here we tested the hypothesis that sympathetic activation contributes to impaired insulin-mediated vasodilation in adult subjects with obesity.

METHODS AND RESULTS

In a randomized crossover study, we used a euglycemic hyperinsulinemic clamp in 12 subjects with obesity to induce forearm arterial vasodilation (forearm blood flow) and microvascular recruitment (contrast-enhanced ultrasonography) during an intrabrachial infusion of saline (control) or phentolamine (sympathetic blockade). Insulin increased forearm blood flow on both study days (from 2.21±1.22 to 4.89±4.21 mL/100 mL per min, =0.003 and from 2.42±0.89 to 7.19±3.35 mL/100 mL per min, =0.002 for the intact and blocked day, respectively). Sympathetic blockade with phentolamine resulted in a significantly greater increase in microvascular flow velocity (∆microvascular flow velocity: 0.23±0.65 versus 2.51±3.01 arbitrary intensity units (AIU/s) for saline and phentolamine respectively, =0.005), microvascular blood volume (∆microvascular blood volume: 1.69±2.45 versus 3.76±2.93 AIU, respectively, =0.05), and microvascular blood flow (∆microvascular blood flow: 0.28±0.653 versus 2.51±3.01 AIU/s, respectively, =0.0161). To evaluate if this effect was not due to nonspecific vasodilation, we replicated the study in 6 subjects with obesity comparing intrabrachial infusion of phentolamine to sodium nitroprusside. At doses that produced similar increases in forearm blood flow, insulin-induced changes in microvascular flow velocity were greater during phentolamine than sodium nitroprusside (%microvascular flow velocity=58% versus 29%, respectively, =0.031).

CONCLUSIONS

We conclude that sympathetic activation impairs insulin-mediated microvascular recruitment in adult subjects with obesity.

摘要

背景

肥胖与胰岛素代谢(葡萄糖摄取)和血管(一氧化氮介导的扩张和微血管募集)作用的抵抗有关。这些血管效应通过增加组织葡萄糖的输送来提高胰岛素敏感性。我们和其他人的研究表明,交感神经激活有助于葡萄糖摄取的胰岛素抵抗。在这里,我们测试了这样一个假设,即交感神经激活有助于肥胖的成年受试者胰岛素介导的血管舒张受损。

方法和结果

在一项随机交叉研究中,我们使用正葡萄糖高胰岛素钳夹技术,在 12 名肥胖受试者中诱导前臂动脉血管舒张(前臂血流量)和微血管募集(对比增强超声),同时在肱动脉内输注生理盐水(对照)或酚妥拉明(交感神经阻滞)。胰岛素在两天的研究中均增加了前臂血流量(从 2.21±1.22 增加到 4.89±4.21 mL/100 mL per min,=0.003 和从 2.42±0.89 增加到 7.19±3.35 mL/100 mL per min,=0.002,分别为完整和阻滞天)。用酚妥拉明进行的交感神经阻滞导致微血管血流速度(微血流速度变化:盐水和酚妥拉明分别为 0.23±0.65 和 2.51±3.01 任意强度单位(AIU/s),=0.005)、微血管血容量(微血流速度变化:盐水和酚妥拉明分别为 1.69±2.45 和 3.76±2.93 AIU,=0.05)和微血管血流(微血流速度变化:盐水和酚妥拉明分别为 0.28±0.653 和 2.51±3.01 AIU/s,=0.0161)的显著增加。为了评估这种作用是否不是由于非特异性血管舒张引起的,我们在 6 名肥胖受试者中复制了这项研究,比较了臂内输注酚妥拉明和硝普钠。在产生相似的前臂血流增加的剂量下,胰岛素诱导的微血管血流速度变化在酚妥拉明期间大于硝普钠(微血流速度变化百分比=58%对 29%,分别,=0.031)。

结论

我们得出结论,交感神经激活会损害肥胖成年受试者的胰岛素介导的微血管募集。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3085/11963928/fde3abe8844e/JAH3-13-e030775-g003.jpg

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