arginine/stroke

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Testing of cerebral endothelium function with L-arginine after stroke.

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BACKGROUND Endothelium-dependent vasodilatation could be impaired during hypoperfusion. L-arginine (L-A), a precursor of nitric oxide, is able to elicit endothelium-dependent vasodilatation. To determine cerebral vascular endothelial function in the early stages after ischemic stroke, we studied

Arginine vasopressin (AVP) expressional changes in the hypothalamic paraventricular and supraoptic nuclei of stroke-prone spontaneously hypertensive rats.

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Arginine vasopressin (AVP) is a neuropeptide with vasoconstrictive, antidiuretic, cardiovascular regulative and hepatic glycogenolysis effects, that also affects other behaviors including modulating learning. A number of studies on AVP regulation have been conducted in various metabolic diseases

L-arginine is effective in stroke-like episodes of MELAS associated with the G13513A mutation.

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We report a case involving a 15-year-old boy with MELAS (G13513A mutation) who developed several stroke-like episodes in a short period of time. Intravenous administration of l-arginine during the acute phase of the stroke-like episodes reduced symptoms immediately, and oral supplementation of

Nitric oxide donors (nitrates), L-arginine, or nitric oxide synthase inhibitors for acute stroke.

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Nitric oxide (NO) has multiple effects that may be beneficial in acute stroke, including lowering blood pressure, and promoting reperfusion and cytoprotection. Some forms of nitric oxide synthase inhibition (NOS-I) may also be beneficial. However, high concentrations of NO are likely to be toxic to

[Usefulness of L-arginine infusion for status epilepticus in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes].

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We encountered an 11-year-old girl with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) who developed occipital lobe epilepsy at the age of 7 years and 4 months. Thereafter she had repeated status epilepticus associated with stroke-like episodes. Status

Neuroprotective effects of NG-nitro-L-arginine in focal stroke in the 7-day old rat.

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Recent evidence in primary neuronal cell culture implicates nitric oxide (NO) as a mediator of glutamatergic neurotoxicity acting via N-methyl-D-aspartate (NMDA) receptors. We find that administration of the potent nitric oxide synthetase (NOS) inhibitor NG-nitro-L-arginine (NO-Arg) at 50 mg/kg to

Evaluation of the secretory pattern of plasma arginine vasopressin in stroke patients.

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Arginine vasopressin (AVP) may play a role in the development of ischemic brain edema and/or cerebral vasospasm. Data available on AVP plasma levels in ischemic stroke are few and discordant. In order to ascertain whether changes in AVP plasma levels occur in ischemic stroke, plasma AVP levels,

L-arginine-mediated vasoreactivity in patients with a risk of stroke.

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OBJECTIVE L-arginine is the substrate for nitric oxide (NO) production and has been shown to induce an endothelium-dependent increase in cerebral blood flow in humans. We studied the hypothesis that L-arginine-mediated vasoreactivity is impaired in patients with cardiovascular risk factors and a

Effects of NG-nitro-L-arginine on alpha-agonists-induced contraction of aortae from Wistar Kyoto rats and stroke-prone spontaneously hypertensive rats.

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Differences in the influences of endothelium-derived nitric oxside (NO) on alpha-agonists-induced contraction in the aortae of spontaneously hypertensive and normotensive rats were studied by blocking NO synthesis with NG-nitro-L-arginine (L-NNA). L-NNA potentiated the contraction induced by

Plasma arginine-vasopressin following experimental stroke: effect of osmotherapy.

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Neurohumoral responses have been implicated in the pathogenesis of ischemia-evoked cerebral edema. In a well-characterized animal model of ischemic stroke, the present study was undertaken to 1) study the profile of plasma arginine-vasopressin (AVP), and 2) determine whether osmotherapy with

Reduction of neuronal damage in ischemic stroke using a combination therapy of TMB-8 with L-arginine.

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Treatment with a combination of a calcium antagonist TMB-8 and NO donors, L-arginine and N alpha-benzoyl-L-arginine ethyl ester (BAEE) to prevent experimental ischemic stroke were studied in rats through the permanent occlusion of the middle cerebral artery and common carotid artery for 60 minutes.

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

Associations between serum L-arginine and ficolins in the early phase of acute ischemic stroke - A pilot study

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rong class="sub-title"> Introduction: rong> Activation of both the L-arginine and the lectin pathway contributes to the pathophysiology and the outcome of acute ischemic stroke (AIS). However, the interplay between the two systems has not yet been examined. rong

Beneficial effect of L-arginine for stroke-like episode in MELAS.

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We here reported the clinical course and therapeutic details of a 16-year-old girl with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) who had had five stroke-like episodes (two episodes were clinically mild, while the three subsequent episodes were

Effect of long-term oral treatment with L-arginine and idebenone on the prevention of stroke-like episodes in an adult MELAS patient.

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BACKGROUND Mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) is a maternally-inherited multisystem disorder. Mitochondrial angiopathy mediated by nitric oxide, a metabolite of L-arginine, is among the proposed pathophysiologic mechanisms of stroke-like episodes (SLEs) in

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