Protective Effects of L-arginine During Reperfusion by Femoropopliteal Bypass for Lower Limb Ischemic Syndrome in Humans
Status:
Completed
Trial end date:
2013-11-01
Target enrollment:
Participant gender:
Summary
The symptoms and severity of arterial disease is secondary to perfusion deficit. The specific
alteration of the mitochondrial function of ischemic skeletal muscle plays an important role,
and therapeutic enhancing mitochondrial function are associated with a clinical improvement
with increase in the walking distance of the patient.
In severe ischemia, reperfusion required is accompanied by a deleterious episode through a
worsening of endothelial dysfunction (impaired pathway of nitric oxide (NO)), majorant
alteration of cellular energy and the hormonal and inflammatory responses. This is
reperfusion syndrome, which can lead to grave consequences. Our goal is to limit
mitochondrial and endothelial dysfunction (increased by the reperfusion) by stimulating the
NO pathway by in situ addition of its precursor, L-arginine. Our working hypothesis is that
this cellular improvement will be accompanied by an increase in systolic pressure index and
an improvement in the walking distance.
Method: This is a trial with direct individual benefit, comparative, randomized, prospective,
single-center, double-blind, versus placebo.