l arginine/infartarse

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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

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

[Protective effect of tetramethylpyrazine and L-arginine on rats with acute myocardial infarction].

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OBJECTIVE To compare the protective effects of tetramethylpyrazine (TMP) alone and TMP and L-arginine (TMP-LA) combination on rats with acute myocardial infarction (AMI), and to explore its mechanism. METHODS The rat model of AMI was established by via caudal vein injection of pituitrin.

Cerebrovascular reactivity to L-arginine in patients with lacunar infarctions.

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BACKGROUND It is well known that endothelial dysfunction plays an important role in the pathogenesis of many cardiovascular disorders. The aim of this study was to test the hypothesis that specific, marked endothelial dysfunction of cerebral arteries is present in patients with lacunar cerebral

Aerobic training and l-arginine supplementation promotes rat heart and hindleg muscles arteriogenesis after myocardial infarction.

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Arteriogenesis is a main defense mechanism to prevent heart and local tissues dysfunction in occlusive artery disease. TGF-β and angiostatin have a pivotal role in arteriogenesis. We tested the hypothesis that aerobic training and l-arginine supplementation promotes cardiac and skeletal muscles

Role of l-Arginine on Dyslipidemic Conditions of Acute Myocardial Infarction Patients.

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Oxidative stress conditions associated with atherosclerosis leads to oxidative modification of low-density lipoprotein (LDL). The body's capabilities to inhibit LDL oxidation and to remove or neutralize the atherogenic oxidized LDL (ox-LDL) are limited. When the LDL cholesterol level increases in

Influence of atorvastatin treatment on L-arginine cerebrovascular reactivity and flow-mediated dilatation in patients with lacunar infarctions.

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OBJECTIVE In our study we hypothesized that statins improve endothelial function in patients with lacunar infarctions (LI). Cerebral and systemic endothelial function was determined before and after 3-months treatment with atorvastatin. METHODS Cerebral endothelial function was determined by

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