Ascorbate improves circulation in postural tachycardia syndrome.

Ascorbate improves circulation in postural tachycardia syndrome.
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抗坏血酸可改善体位性心动过速综合征的血液循环。

DOI:
10.1152/ajpheart.00018.2011
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发表时间:
2011
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
--
通讯作者:
Medow,MarvinS
Medow,MarvinS
中科院分区:
--
文献类型:
--
作者:
Stewart,JulianM;Ocon,AnthonyJ;Medow,MarvinS

文献摘要

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低流量体位性心动过速综合征(LFP)与血管收缩、心输出量减少、血浆血管紧张素II升高、生物可利用一氧化氮(NO)降低和氧化应激有关。我们测试了抗坏血酸是否会改善皮肤一氧化氮并减少全身血管收缩。我们采用局部皮肤加热至42°C和激光多普勒血流仪来评估11名LFP患者和8名对照受试者(年龄23±2岁)对抗坏血酸钠的no依赖电导(%CVCmax)和对抗坏血酸的全身血流动力学反应。我们向皮内微透析导管灌注抗坏血酸钠(10mm)或林格氏溶液。LFP的药前热反应降低,特别是no依赖平台期(56±6 vs 88±7%CVCmax)。抗坏血酸增加了LFP和对照组受试者的基线皮肤流量,并增加了LFP平台反应(82±6 vs 92±6对照)。全身输注实验采用Finometer和ModelFlow估计相对心脏指数(CI),前臂和小腿静脉闭塞容积描记术估计输注抗坏血酸前后的血流量、外周动脉和静脉阻力以及电容。抗坏血酸后CI增加了40%,外周血流也增加了40%。服用抗坏血酸后,外周阻力增加(几乎是对照组的两倍),下降了近50%。与对照组相比,小腿电容和静脉阻力下降,但抗坏血酸使其恢复正常。这些数据为氧化应激和一氧化氮减少可能导致LFP血管收缩和静脉收缩的概念提供了实验支持。
Low flow postural tachycardia syndrome (LFP) is associated with vasoconstriction, reduced cardiac output, increased plasma angiotensin II, reduced bioavailable nitric oxide (NO), and oxidative stress. We tested whether ascorbate would improve cutaneous NO and reduce vasoconstriction when delivered systemically. We used local cutaneous heating to 42°C and laser Doppler flowmetry to assess NO-dependent conductance (%CVCmax) to sodium ascorbate and the systemic hemodynamic response to ascorbic acid in 11 LFP patients and in 8 control subjects (aged 23 ± 2 yr). We perfused intradermal microdialysis catheters with sodium ascorbate (10 mM) or Ringer solution. Predrug heat response was reduced in LFP, particularly the NO-dependent plateau phase (56 ± 6 vs. 88 ± 7%CVCmax). Ascorbate increased baseline skin flow in LFP and control subjects and increased the LFP plateau response (82 ± 6 vs. 92 ± 6 control). Systemic infusion experiments used Finometer and ModelFlow to estimate relative cardiac index (CI) and forearm and calf venous occlusion plethysmography to estimate blood flows, peripheral arterial and venous resistances, and capacitance before and after infusing ascorbic acid. CI increased 40% after ascorbate as did peripheral flows. Peripheral resistances were increased (nearly double control) and decreased by nearly 50% after ascorbate. Calf capacitance and venous resistance were decreased compared with control but normalized with ascorbate. These data provide experimental support for the concept that oxidative stress and reduced NO possibly contribute to vasoconstriction and venoconstriction of LFP.