Restoring vascular nitric oxide formation by L-arginine improves the symptoms of intermittent claudication in patients with peripheral arterial occlusive disease
Rainer H. Böger, MD*,
Stefanie M. Bode-Böger, MD*,
Wolfgang Thiele*,
Andreas Creutzig, MD ,
Klaus Alexander, MD and
J.ürgen C. Frölich, MD*
* Institute of Clinical Pharmacology, Hannover Medical School, Hannover, Germany
Department of Angiology, Hannover Medical School, Hannover, Germany
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Figure 1 Effect of intravenous infusion therapy with L-arginine or PGE1 on the pain-free (a) and absolute walking distance (b) in patients with chronic stable intermittent claudication. Data are mean ± SEM. *p < 0.05.
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Figure 2 Changes of femoral artery diameter during the hyperemic reaction induced by 3 min of suprasystolic occlusion before, during and after 3 weeks of infusion therapy with L-arginine (a), PGE1 (b), or in control patients (c), as well as 6 weeks after the end of the active treatment period. Data are mean ± SEM.
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Figure 3 Bar graphs showing peak femoral artery flow (ml/min), increase in femoral artry diameter (as percent of baseline diameter) during reactive hyperemia before and after 3 weeks of intermittent infusion therapy with L-arginine or PGE1, and in control patients. The area under the curve (AUC, arbitrary units) of femoral artery flow during hyperemia and the time elapsing between peak hyperemia and return to 50% of this peak (t1/2, s) are also shown. Data are mean ± SEM. *p < 0.05 vs. baseline. Striped columns = baseline; solid columns = 3 weeks.
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Figure 4 Urinary excretion rates of nitrate (a) and cGMP (b) in patients with chronic intermittent claudication before, during and after 3 weeks of infusion therapy with L-arginine or PGE1, and in control patients. Data are mean ± SEM. *p < 0.05.
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