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Microvascular Permeability after an Acute and Chronic Salt Load in Healthy Subjects: A Randomized Open-label Crossover Intervention Study
背景与目的
钠引起的微循环改变，尤其是内皮表层的改变，可能在钠介导的血压升高中起着重要作用。然而，急性和慢性钠负荷对人内皮表层和微循环的影响尚未确定。这项研究的目的是将钠引起的血压及体重的变化作为主要评估结果，其他还包括微血管通透性、舌下微循环和健康志愿者尿糖胺聚糖的排泄。
方 法
12名血压正常的男性按随机分为8天低钠饮食(小于50 mmol/天)和高钠饮食(超过200 mmol/天)组。低钠饮食后，30分钟内静脉给予高渗盐水(5毫摩尔钠/升身体水)。高渗生理盐水(含钠5mmol/L)30 min内静脉给药。
结 果
两种干预措施都没有改变血压。钠负荷膳食后体重增加2.5(95%CI，1.7至3.2)kg（P < 0.001），急性静脉钠负荷用量增加了125I-标记的白蛋白的毛细血管漏出率（2.7 [0.1 to 5.3] % cpm · g−1 · h–1; P = 0.04）；尽管血浆钠含量和渗透压有类似的增加，慢性钠负荷膳食没有影响125I标记的白蛋白的漏出率（−0.03 [−3.3 to 3.2] % cpm · g−1 · h–1; P = 1.00）。急性静脉钠负荷用量伴随血浆体积显著增加（根据白蛋白的分布量来评估）并显著降低硫酸肝素和硫酸软骨素的尿排出量，这些变化在钠负荷饮食中没有被观察到。
结 论
静脉钠负荷对内皮细胞表层有直接的不良影响，而不影响血压。
原始文献摘要
Nmg R, Rhg O E, Chahid Y, et al. Microvascular Permeability after an Acute and Chronic Salt Load in Healthy Subjects: A Randomized Open-label Crossover Intervention Study[J]. Anesthesiology, 2017:1.
Background:Sodium-induced microcirculatory changes, endothelial surface layer alterations in particular, may play an important role in sodium-mediated blood pressure elevation. However, effects of acute and chronic sodium loading on the endothelial surface layer and microcirculation in humans have not been established. The objective of this study was to assess sodium-induced changes in blood pressure and body weight as primary outcomes and also in microvascular permeability, sublingual microcirculatory dimensions, and urinary glycosaminoglycan excretion in healthy subjects.
Methods: Twelve normotensive males followed both a low-sodium diet (less than 50 mmol/day) and a high-sodium diet (more than 200 mmol/day) for eight days in randomized order, separated by a crossover period. After the low-sodium diet, hypertonic saline (5 mmol sodium/liter body water) was administered intravenously in 30 min.
Results: Both sodium interventions did not change blood pressure. Body weight increased with 2.5 (95% CI, 1.7 to 3.2) kg (P < 0.001) after dietary sodium loading. Acute intravenous sodium loading resulted in increased transcapillary escape rate of 125I-labeled albumin (2.7 [0.1 to 5.3] % cpm · g−1 · h–1; P = 0.04), whereas chronic dietary sodium loading did not affect transcapillary escape rate of 125I-labeled albumin (−0.03 [−3.3 to 3.2] % cpm · g−1 · h–1; P = 1.00), despite similar increases of plasma sodium and osmolality. Acute intravenous sodium loading coincided with significantly increased plasma volume, as assessed by the distribution volume of albumin, and significantly decreased urinary excretion of heparan sulfate and chondroitin sulfate. These changes were not observed after dietary sodium loading.
Conclusions: Our results suggest that intravenous sodium loading has direct adverse effects on the endothelial surface layer, independent of blood pressure.
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