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Controlled Clinical Trial
. 2011 Sep;301(3):H1033-42.
doi: 10.1152/ajpheart.00018.2011. Epub 2011 May 27.

Ascorbate Improves Circulation in Postural Tachycardia Syndrome

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Free PMC article
Controlled Clinical Trial

Ascorbate Improves Circulation in Postural Tachycardia Syndrome

Julian M Stewart et al. Am J Physiol Heart Circ Physiol. .
Free PMC article

Abstract

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 (%CVC(max)) 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%CVC(max)). 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.

Figures

Fig. 1.
Fig. 1.
Representative supine leg plethysmographic tracing. Ascending portion of the volume-pressure relation was generated using 10-mmHg pressure increments beginning at 20 mmHg as shown at top. Bottom left: curve stripping method used to separate intravascular filling from capillary filtration. Bottom right: decrease in limb blood volume that occurs immediately following the release of occlusion cuff pressure (at 60 mmHg). Initial flow is fit by a straight line and used to compute venous resistance.
Fig. 2.
Fig. 2.
Heating response expressed as percent maximum conductance (%CVCmax) before and after administration of sodium ascorbate in control subjects (left) and in postural tachycardia syndrome (POTS) patients (right.). Data obtained before ascorbate is shown in black; data obtained after ascorbate perfusion is shown in gray. Ascorbate caused an increase in baseline conductance in POTS and control subjects alike. There was no affect of ascorbate on control plateau. Before ascorbate, POTS heating response was diminished compared with control but was significantly increased after ascorbate.
Fig. 3.
Fig. 3.
Volume-pressure data points from supine POTS (gray) and control (black) subjects obtained from the forearm (top) and calf (bottom). Data were obtained before ascorbate infusion. Data for the forearm were similar for POTS and control while there was a significantly reduced calf volume at given pressure for POTS and thus decreased vascular capacitance. *P < 0.05, compared with control.
Fig. 4.
Fig. 4.
Changes in mean arterial pressure (MAP; top left) and heart rate (HR; bottom left) and relative measures of cardiac output (CO; top right) and total peripheral resistance (TPR; bottom right) in a representative POTS patient during the ascorbate infusion. Initiation of ascorbate infusion is indicated by the arrows. Woods U, Woods units; bpm, beats/min.
Fig. 5.
Fig. 5.
Percent changes in regional blood volumes produced by the infusion of ascorbic acid. There was a significant increase in thoracic blood volume in POTS with reciprocal decreases in splanchnic, pelvic, and leg blood volumes. Significant changes were not observed in controls. *P < 0.05, compared with zero.
Fig. 6.
Fig. 6.
Volume-pressure relationship for forearms (top) and calfs (bottom) in POTS patients (right) and control subjects (left). Data obtained before ascorbate (“pre-Asc”) are shown in black and after ascorbate (“post-Asc”) are shown in gray. On average, capacitance increased in forearms and markedly increased in calfs for POTS but not control subjects after ascorbate. *P < 0.05, compared with control.

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