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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) 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
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 (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
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
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
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,
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
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
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
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.
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
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.
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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
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