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动脉内输注胰岛素可减弱人前臂的血管反应性。

Intra-arterial infusion of insulin attenuates vasoreactivity in human forearm.

作者信息

Sakai K, Imaizumi T, Masaki H, Takeshita A

机构信息

Cardiology Section, National Fukuoka Hospital, Japan.

出版信息

Hypertension. 1993 Jul;22(1):67-73. doi: 10.1161/01.hyp.22.1.67.

DOI:10.1161/01.hyp.22.1.67
PMID:8319994
Abstract

Hyperinsulinemia may contribute to the development of hypertension. The aim of the present study was to determine whether hyperinsulinemia modulates vascular reactivity to phenylephrine or angiotensin II. In 10 young, healthy volunteers, the left brachial artery was cannulated for drug infusion and direct measurements of arterial pressure. We measured forearm blood flow by a strain-gauge plethysmograph while infusing phenylephrine (0.2, 0.8, and 2.4 micrograms/min) and angiotensin II (5, 10, and 20 ng/min) locally into the brachial artery before and during simultaneous intra-arterial infusion of insulin (0.15 mU/kg per minute). Forearm vascular resistance was calculated from directly measured arterial pressure and forearm blood flow. Intra-arterial infusion of insulin raised the local plasma insulin level from 10.3 +/- 1.4 to 133.3 +/- 21.1 microU/mL (P < .01) and did not change blood glucose level in the venous effluents of the forearm. Insulin infusion slightly but not significantly increased basal forearm blood flow (4.6 +/- 1.5 to 5.5 +/- 0.9 mL/min per 100 milliliters, NS) and decreased forearm vascular resistance (22.1 +/- 2.1 to 20.3 +/- 2.8 U, NS). Phenylephrine and angiotensin II increased forearm vascular resistance dose dependently before and during simultaneous insulin infusion (P < .01 for both). Intra-arterial infusion of insulin attenuated vascular reactivity to phenylephrine (P < .01) and angiotensin II (P < .01). None of these drugs changed blood pressure or heart rate. Our results suggest that hyperinsulinemia attenuates vascular reactivity in the forearm resistance vessels in healthy humans.

摘要

高胰岛素血症可能促使高血压的发生。本研究的目的是确定高胰岛素血症是否会调节血管对去氧肾上腺素或血管紧张素II的反应性。在10名年轻健康志愿者中,将左肱动脉插管用于药物输注和直接测量动脉压。在动脉内同时输注胰岛素(每分钟0.15 mU/kg)之前和期间,我们通过应变片体积描记器测量前臂血流量,同时将去氧肾上腺素(0.2、0.8和2.4微克/分钟)和血管紧张素II(5、10和20纳克/分钟)局部注入肱动脉。根据直接测量的动脉压和前臂血流量计算前臂血管阻力。动脉内输注胰岛素使局部血浆胰岛素水平从10.3±1.4微单位/毫升升至133.3±21.1微单位/毫升(P<.01),且未改变前臂静脉流出液中的血糖水平。胰岛素输注使基础前臂血流量略有增加但无显著差异(从每100毫升4.6±1.5毫升/分钟增至5.5±0.9毫升/分钟,无统计学意义),并降低了前臂血管阻力(从22.1±2.1单位降至20.3±2.8单位,无统计学意义)。在同时输注胰岛素之前和期间,去氧肾上腺素和血管紧张素II均剂量依赖性地增加前臂血管阻力(两者P<.01)。动脉内输注胰岛素减弱了血管对去氧肾上腺素(P<.01)和血管紧张素II(P<.01)的反应性。这些药物均未改变血压或心率。我们的结果表明,高胰岛素血症会减弱健康人前臂阻力血管的血管反应性。

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