Blood pressure and hemodynamic responses to an acute sodium load in humans
Blood pressure and hemodynamic responses to an acute sodium load in humans
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DOI：
10.1152/japplphysiol.00262.2005
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发表时间：
2005-10-01
影响因子：
3.3
通讯作者：
Stillabower, ME
中科院分区：
文献类型：
--
作者：
Farquhar, WB;Paul, EE;Stillabower, ME
本研究旨在探讨氯化钠（3%静脉注射液）对急性血压（BP）和血流动力学的影响。虽然许多研究将饮食中钠的变化与血压的变化联系起来，但很少有人考虑血液中钠浓度对血压的影响。我们假设静脉内钠负荷会增加血压，并量化了心输出量（（Q）与点c）和外周血管阻力（PVR）的变化。13名受试者（年龄27 ± 2岁）接受了60分钟3%生理盐水输注（0.15 ml中心点kg（-1）中心点min（-1））。使用Finometer逐搏评估BP，通过CO2再呼吸技术评估C点上的（Q），并推导PVR。输注过程中血钠和渗透压升高，红细胞压积下降（ANOVA，P < 0.01）。平均动脉压（MAP）在输注期间从81.8 +/- 3.4持续增加至91.6 +/- 3.6 mmHg（ANOVA，P < 0.01）。血压对钠的反应性表示为血清钠-MAP关系的斜率，平均值为1.75 +/- 0.34 mmHg中心点mmol（-1）中心点l（-1）。血压对容积变化的反应性表示为血细胞比容-MAP关系的斜率，平均值为-2.2 +/- 0.35 mmHg/%。MAP的早期变化是由（Q）超过点c的增加介导的，晚期变化是由PVR的增加介导的（P < 0.05），对应于血浆去甲肾上腺素增加30%。总之，高渗盐水急性输注可有效升高血压，钠和容量似乎都参与了这一升高;可使用MAP-钠图量化急性血压对血清钠的反应性。
The purpose of this study was to investigate the acute blood pressure (BP) and hemodynamic effects of sodium chloride (3% intravenous solution). Although many studies link a change in dietary sodium to a change in BP, few consider the effects of sodium concentration in the blood on BP. We hypothesized that an intravenous sodium load would increase BP, and we quantified alterations in cardiac output ((Q) over dot c) and peripheral vascular resistance (PVR). Thirteen subjects (age 27 +/- 2 yr) underwent a 60-min 3% saline infusion (0.15 ml center dot kg(-1) center dot min(-1)). BP was assessed on a beat-to-beat basis with a Finometer, (Q) over dot c was assessed via the CO2 rebreathing technique, and PVR was derived. Serum sodium and osmolality increased, and hematocrit declined during the infusion (ANOVA, P < 0.01). Mean arterial pressure (MAP) increased continuously during the infusion from 81.8 +/- 3.4 to 91.6 +/- 3.6 mmHg (ANOVA, P < 0.01). BP responsiveness to sodium was expressed as the slope of the serum sodium-MAP relationship and averaged 1.75 +/- 0.34 mmHg center dot mmol(-1) center dot l(-1). BP responsiveness to the volume change was expressed as the slope of the hematocrit-MAP relationship and averaged -2.2 +/- 0.35 mmHg/%. The early change in MAP was mediated by an increase in (Q) over dot c and the late change by an increase in PVR (P < 0.05), corresponding to a 30% increase in plasma norepinephrine. In conclusion, an acute infusion of hypertonic saline was effective in increasing BP, and both sodium and volume appear to be involved in this increase; acute BP responsiveness to serum sodium can be quantified using a MAP-sodium plot.