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Effect of ranolazine on plasma arginine derivatives and urinary isoprostane 8-iso-PGF2α in patients with myocardial infarction in the randomized RIMINI-Trial.
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The purpose of the present study was to assess whether 6-week ranolazine application on top of guideline-based treatment impacts on the arginine/NO pathway and urinary isoprostane 8-iso-PGF2α as marker of oxidative stress in patients directly after a myocardial infarction. 20 patients
L-arginine therapy in acute myocardial infarction: the Vascular Interaction With Age in Myocardial Infarction (VINTAGE MI) randomized clinical trial.
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BACKGROUND
The amino acid L-arginine is a substrate for nitric oxide synthase and is increasingly used as a health supplement. Prior studies suggest that L-arginine has the potential to reduce vascular stiffness.
OBJECTIVE
To determine whether the addition of L-arginine to standard postinfarction
Aerobic training and L-arginine supplement attenuates myocardial infarction-induced kidney and liver injury in rats via reduced oxidative stress.
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BACKGROUND
The aim of the present study was to determine the effect of exercise training and l-arginine supplementation on kidney and liver injury in rats with myocardial infarction (MI).
METHODS
Four weeks after MI, 50 male wistar rats randomly divided into five followed groups: sham surgery
Poly-arginine peptides reduce infarct volume in a permanent middle cerebral artery rat stroke model.
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We recently reported that poly-arginine peptides have neuroprotective properties both in vitro and in vivo. In cultured cortical neurons exposed to glutamic acid excitotoxicity, we demonstrated that neuroprotective potency increases with polymer length plateauing at R15 to R18 (R = arginine
Retrograde infusion of lidocaine or L-arginine before reperfusion reduces myocardial infarct size.
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BACKGROUND
Retrograde perfusion preserves ischemic myocardium when initiated shortly after coronary artery occlusion. However, benefits diminish as the delay increases. In this study, we used this technique to deliver agents known to reduce the injury associated with the reperfusion of ischemic
[Ischemic preconditioning and exogenous L-arginine reduce infarct size in rabbit heart].
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The effects of NO donor--L-arginine (L-arg) and ischemic preconditioning (IP) on the hemodynamics and myocardial infarct size were examined in the anesthetized rabbit subjected to myocardial ischemia-repefusion to define whether exogenous L-arg could exert a beneficial effect in this pathological
L-arginine decreases infarct size in rats exposed to environmental tobacco smoke.
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This study examined the effects of L-arginine on myocardial infarct size, hemodynamics, and vascular reactivity in environmental tobacco smoke (ETS)-exposed and non-ETS-exposed rats. We previously demonstrated that exposure to ETS increased myocardial infarct size in a rat model of ischemia and
Blockade of nitric oxide formation by N omega-nitro-L-arginine mitigates ischemic brain edema and subsequent cerebral infarction in rats.
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In order to investigate whether or not nitric oxide (NO) formation underlies the cellular mechanisms of ischemic brain damage, we examined the effects of N omega-nitro-L-arginine (L-NNA), a NO synthase inhibitor, on ischemic brain edema and subsequent infarction in rats with middle cerebral artery
Cardioprotective activity of placental growth factor combined with oral supplementation of l-arginine in a rat model of acute myocardial infarction.
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OBJECTIVE
Exogenous administration of placental growth factor (PlGF) stimulates angiogenesis and improves ventricular remodeling after acute myocardial infarction (AMI), and supplementation with l-arginine ameliorates endothelial function. The objective of the present study was to compare the
Oral L-arginine supplementation in acute myocardial infarction therapy: a meta-analysis of randomized controlled trials.
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OBJECTIVE
The objective was to analyze completed trials assessing the effect of oral L-arginine supplementation on clinical outcomes of patients with acute myocardial infarction (AMI).
BACKGROUND
Prior trials suggest that oral L-arginine administration improves endothelial function in patients with
Effect of L-arginine oral supplementation on response to myocardial infarction in hypercholesterolemic and hypertensive rats.
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The well known metabolic functions of L-arginine have been recently increased with the discovery of its role as the substrate for the synthesis of nitric oxide (NO), which has emerged as an endogenous signaling molecule with potential therapeutic implications for cardiovascular disease. Steady-state
L-Arginine administration prevents reperfusion-induced cardiomyocyte hypercontracture and reduces infarct size in the pig.
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OBJECTIVE
Stimulation of cGMP synthesis protects cardiomyocytes against reoxygenation-induced hypercontracture. The purpose of this study was to determine whether L-arginine supplementation has a protective effect against reperfusion-induced hypercontracture and necrosis in the intact
Efficacy and safety of oral l-arginine in acute myocardial infarction. Results of the multicenter, randomized, double-blind, placebo-controlled ARAMI pilot trial.
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OBJECTIVE
L-arginine is a substrate for nitric oxide (NO) synthesis in vascular endothelial cells. NO bioavailability is decreased during myocardial infarction (MI). It might be expected that administration of L-arginine may maintain NO production and alleviate the course of MI. The aim of the study
Intracoronary L-arginine during reperfusion improves endothelial function and reduces infarct size.
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We tested the hypothesis that intracoronary administration of L-arginine (L-Arg), the physiological nitric oxide (NO) precursor, during reperfusion would attenuate postischemic damage by L-Arg NO-pathway mechanisms. Open-chest, anesthetized dogs underwent 60 min of left anterior descending coronary
L-arginine ameliorates cerebral blood flow and metabolism and decreases infarct volume in rats with cerebral ischemia.
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Effects of L-arginine, 300 mg/kg, i.p., on the regional cerebral blood flow (rCBF), brain metabolism, and infarct volume were examined in spontaneously hypertensive rats subjected to occlusion of both left middle cerebral artery and left common carotid artery. Rats treated with L-arginine had higher
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