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硝酸甘油急性降低血压并不能使原发性高血压患者的大动脉僵硬度恢复正常。

Acute reduction of blood pressure by nitroglycerin does not normalize large artery stiffness in essential hypertension.

作者信息

Stewart Andrew D, Jiang Benyu, Millasseau Sandrine C, Ritter James M, Chowienczyk Philip J

机构信息

Cardiovascular Division, King's College London School of Medicine, St Thomas' Hospital, London, United Kingdom.

出版信息

Hypertension. 2006 Sep;48(3):404-10. doi: 10.1161/01.HYP.0000237669.64066.c5. Epub 2006 Aug 14.

DOI:10.1161/01.HYP.0000237669.64066.c5
PMID:16908758
Abstract

Stiffness of large elastic arteries is elevated in subjects with hypertension, an effect that could potentially be explained by increased distending pressure. We examined effects of an acute change in blood pressure on carotid-femoral pulse wave velocity and carotid artery distensibility (inversely related to stiffness) in normotensive control subjects (n=20, mean age 42) with mean arterial pressure (MAP) 84+/-1.7 mm Hg (mean+/-SE) and subjects with essential hypertension (n=20, mean age 45, MAP 104+/-2.0 mm Hg). Normotensive subjects received intravenous nitroglycerin (NTG) and angiotensin II to lower/increase blood pressure. Hypertensive subjects received NTG to lower blood pressure. Pulse wave velocity was 24% (95% CI: 12% to 35%) higher and carotid distensibility 47% (95% CI: 32% to 63%) lower in hypertensive subjects compared with controls. In normotensive subjects, acute changes in blood pressure produced expected changes in stiffness. However, in hypertensive subjects, despite reducing MAP by 22 mm Hg to the same level as in normotensive subjects, there was no detectable reduction in arterial stiffness: pulse wave velocity remained 24% (95% CI: 10% to 38%) higher and carotid distensibility 48% (95% CI: 31% to 63%) lower in hypertensive compared with normotensive subjects. Because blood pressure-independent effects of NTG are, if anything, to reduce stiffness, these results indicate that elevated carotid and aortic stiffness in hypertensive subjects is not explained by elevated blood pressure but relates to structural change in the arterial wall.

摘要

高血压患者的大弹性动脉僵硬度升高,这种效应可能由扩张压力增加来解释。我们研究了血压急性变化对正常血压对照受试者(n = 20,平均年龄42岁,平均动脉压[MAP] 84±1.7 mmHg[均值±标准误])和原发性高血压患者(n = 20,平均年龄45岁,MAP 104±2.0 mmHg)的颈股脉搏波速度和颈动脉扩张性(与僵硬度呈负相关)的影响。正常血压受试者接受静脉注射硝酸甘油(NTG)和血管紧张素II以降低/升高血压。高血压患者接受NTG以降低血压。与对照组相比,高血压患者的脉搏波速度高24%(95%置信区间:12%至35%),颈动脉扩张性低47%(95%置信区间:32%至63%)。在正常血压受试者中,血压的急性变化产生了预期的僵硬度变化。然而,在高血压患者中,尽管将MAP降低22 mmHg至与正常血压受试者相同的水平,但未检测到动脉僵硬度降低:与正常血压受试者相比,高血压患者的脉搏波速度仍高24%(95%置信区间:10%至38%),颈动脉扩张性低48%(95%置信区间:31%至63%)。由于NTG对血压的独立影响,如果有的话,是降低僵硬度,这些结果表明高血压患者颈动脉和主动脉僵硬度升高并非由血压升高所致,而是与动脉壁的结构变化有关。

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