Key result
IV lipid infusion increases sympathetic-vascular transduction ~38%, an effect attenuated by coinfused ascorbic acid.
Why the study?
Elevated circulating lipids increase oxidative stress and impair vascular function, but their effects on sympathetic-vascular control in humans are not well understood.
Does coinfusion of ascorbic acid prevent lipid-induced enhancement of sympathetic-vascular transduction and arterial pressure variability in healthy adults?
RCT (n=26)
Double-blind
Randomized
No
Does coinfusion of ascorbic acid prevent lipid-induced enhancement of sympathetic-vascular transduction and arterial pressure variability in healthy adults?
Absolute Event Rate: 4.7% vs 3.4%
p-value: p=0.03
Intravenous lipid infusion acutely enhances sympathetic-vascular transduction and blood pressure variability via oxidative stress, which can be mitigated by the antioxidant ascorbic acid.
Ascorbic acid coinfusion mitigates lipid-enhanced sympathetic-vascular transduction; extends causal RCT evidence for oxidative stress in blood pressure regulation.
BACKGROUND: Elevated circulating lipids increase oxidative stress and impair vascular function, but their effects on sympathetic-vascular control in humans are not well understood. We tested the hypothesis that intravenous lipid infusion enhances sympathetic-vascular transduction and beat-to-beat arterial pressure variability in humans, and that these effects are mediated, in part, by oxidative stress. METHODS: In a randomized, double-blind, placebo-controlled crossover study, healthy adults underwent 2 hours of intravenous lipid infusion (20% Intralipid) with coinfusion of ascorbic acid or saline control. Endothelial function was assessed by brachial artery flow-mediated dilation, and muscle sympathetic nerve activity (MSNA) was recorded using microneurography. Sympathetic-vascular transduction was quantified by signal-averaging beat-to-beat mean arterial pressure (MAP) and brachial vascular conductance responses after spontaneous MSNA bursts. RESULTS: Plasma malondialdehyde increased during lipid+saline (peak: 48±12 versus BL: 42±11 ng/mL; P <0.01) and decreased with lipid+ascorbic acid (nadir: 34±12 versus baseline: 45±14 ng/mL; P <0.01). Lipid+saline reduced flow-mediated dilation (4.1±2.7 versus baseline: 6.8±3.2%; P <0.01), increased beat-to-beat MAP variability (1.7±0.5 versus baseline: 1.5±0.4 mm Hg; P =0.01), and augmented responses to large MSNA bursts for MAP (4.7±2.0 versus baseline: 3.4±1.4%; P =0.03) and vascular conductance (-9.3±3.4 versus BL: −6.7±3.7%; P =0.01). Despite lipid-mediated increases in MSNA burst amplitude, coinfusion of ascorbic acid was not associated with an increase in beat-to-beat MAP variability (1.6±0.4 versus baseline: 1.5±0.4 mm Hg; P =0.23) and MAP (4.4±0.9 versus baseline: 4.1±0.8%; P =0.37) and vascular conductance (−6.8±4.6 versus baseline: −9.4±5.5%; P <0.01) responses to large MSNA bursts, although reductions in flow-mediated dilation were observed (5.0±3.0 versus baseline: 8.1±3.8%; P <0.01). CONCLUSIONS: Lipid infusion enhances sympathetic-vascular transduction and arterial pressure variability, consistent with a redox-sensitive mechanism, while impairing endothelial function via pathways that ascorbic acid does not fully reverse. REGISTRATION: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT04832009.
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Miller et al. (2026) conducted an RCT in Healthy adults (n=26). Intravenous lipid infusion (20% Intralipid) + saline vs. Baseline was evaluated on Mean arterial pressure (MAP) response to large muscle sympathetic nerve activity (MSNA) bursts (p=0.03). Intravenous lipid infusion significantly augmented mean arterial pressure responses to large muscle sympathetic nerve activity bursts compared to baseline (4.7% vs 3.4%), an effect that was attenuated by coinfusion of ascorbic acid.
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