Why the study?
Does nitric oxide contribute to reactive hyperemia, and does L-arginine improve reactive hyperemia in patients with atherosclerosis or endothelial dysfunction?
Population
44 human subjects, comprising 15 normal control subjects without risk factors for atherosclerosis and 29…
Comparison
Intrafemoral arterial NG-monomethyl-L-arginine… vs Baseline measurements and comparison between…
Design
Other
Key result
L-NMMA significantly inhibited reactive hyperemia in normal controls (P=0.0011) but not in patients with atherosclerosis or risk factors, demonstrating abnormal nitric oxide bioactivity.
Authors
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Supports loss of NO-mediated reactive hyperemia in atherosclerosis; leaves open whether L-arginine or NO-targeted therapies alter clinical outcomes.
Case-Control (n=44)
Does nitric oxide contribute to reactive hyperemia, and does L-arginine improve reactive hyperemia in patients with atherosclerosis or endothelial dysfunction?
p-value: p=0.0011
Nitric oxide contributes to reactive hyperemia in the normal human peripheral vasculature, but this NO bioactivity is diminished in patients with atherosclerosis and is not improved by acute L-arginine administration.
Dakak et al. (1998) conducted a case-control in Atherosclerosis and endothelial dysfunction (n=44). L-NMMA and L-arginine vs. Normal controls vs patients with atherosclerosis was evaluated on Inhibition of reactive hyperemia by L-NMMA (p=0.0011). L-NMMA significantly inhibited reactive hyperemia in normal controls (P=0.0011) but not in patients with atherosclerosis or risk factors, demonstrating abnormal nitric oxide bioactivity.