L-arginine induces nitric oxide-dependent vasodilation in patients with critical limb ischemia : a randomized, controlled study

L-Arginine is the precursor of endogenous nitric oxide (NO), which is a potent vasodilator acting via the intracellular second-messenger cGMP. In healthy humans, L-arginine induces peripheral vasodilation and inhibits platelet aggregation due to an increased NO production. Prostaglandin E1 (PGE1) in...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 1996, Vol.93 (1), p.85-90
Hauptverfasser: BODE-BÖGER, S. M, BÖGER, R. H, ALFKE, H, HEINZEL, D, TSIKAS, D, CREUTZIG, A, ALEXANDER, K, FRÖLICH, J. C
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Sprache:eng
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Zusammenfassung:L-Arginine is the precursor of endogenous nitric oxide (NO), which is a potent vasodilator acting via the intracellular second-messenger cGMP. In healthy humans, L-arginine induces peripheral vasodilation and inhibits platelet aggregation due to an increased NO production. Prostaglandin E1 (PGE1) induces peripheral vasodilation via stimulating prostacyclin receptors. We investigated the effects of one intravenous infusion of L-arginine (30 g, 60 minutes) or PGE1 (40 microgram, 60 minutes) versus those of placebo (150 mL 0.9% saline, 60 minutes) on blood pressure, peripheral hemodynamics, and urinary NO3- and cGMP excretion rates in patients with critical limb ischemia (peripheral arterial occlusive disease stages Fontaine III or IV). Blood flow in the femoral artery was significantly increased by L-arginine (+42.3 +/- 7.9%, P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.CIR.93.1.85