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guanidine/accident vasculaire cérébral
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In vitro evaluation of guanidine analogs as sigma receptor ligands for potential anti-stroke therapeutics.
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Currently, the only Food and Drug Administration-approved treatment of acute stroke is recombinant tissue plasminogen activator, which must be administered within 6 hours after stroke onset. The pan-selective σ-receptor agonist N,N'-di-o-tolyl-guanidine (o-DTG) has been shown to reduce infarct
Molecular determinants of Hv1 proton channel inhibition by guanidine derivatives.
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The voltage-gated proton channel Hv1 plays important roles in proton extrusion, pH homeostasis, and production of reactive oxygen species in a variety of cell types. Excessive Hv1 activity increases proliferation and invasiveness in cancer cells and worsens brain damage in ischemic stroke. The
Copper-catalyzed guanidinylation of aryl iodides: the formation of N,N'-disubstituted guanidines.
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A copper-catalyzed cross-coupling reaction of guanidine nitrate with aryl iodides was used for the formation of N,N'-disubstituted guanidines to be used as potential therapeutics for strokes. A relatively inexpensive commercially available guanidine salt and a series of aryl iodides together with
Comparison of vasopressor effects of nitro arginine in stroke-prone spontaneously hypertensive rats and Wistar-Kyoto rats.
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1. NG-nitro-L-arginine (NO2Arg) is a guanidine nitro arginine derivative and an inhibitor of endothelium-dependent vascular relaxation. Significant rise of the systolic blood pressure was observed after 1 week administration of NO2Arg in food (0.023% in weight, about 2.8 mg of NO2Arg/rat per day) in
Subtype-specific modulation of acid-sensing ion channel (ASIC) function by 2-guanidine-4-methylquinazoline.
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Acid-sensing ion channels (ASICs) are neuronal Na(+)-selective channels that are transiently activated by extracellular acidification. ASICs are involved in fear and anxiety, learning, neurodegeneration after ischemic stroke, and pain sensation. The small molecule 2-guanidine-4-methylquinazoline
Creatine salts provide neuroprotection even after partial impairment of the creatine transporter.
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Creatine, a compound that is critical for energy metabolism of nervous cells, crosses the blood-brain barrier (BBB) and the neuronal plasma membrane with difficulty, and only using its specific transporter. In the hereditary condition where the creatine transporter is defective (creatine transporter
Prolinamide derivatives as thrombin inhibitors for the treatment of thrombin-mediated diseases: a patent evaluation of US2013296245.
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BACKGROUND
Thrombotic disorders can lead to deep vein thrombosis, myocardial infarction and stroke. Thrombin plays a vital role in cascade reaction of blood coagulation, inhibition of the activity of thrombin can block the formation of thrombus and direct thrombin inhibitor has a prospect to
Factors affecting the stability and conformation of Locusta migratoria apolipophorin III.
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Apolipophorin III (apoLp-III) from the migratory locust, Locusta migratoria, represents the only full-length apolipoprotein whose three-dimensional structure has been solved. In the present study, spectroscopic methods have been employed to investigate the effects of deglycosylation (via
Synthesis and structure-activity studies of N,N'-diarylguanidine derivatives. N-(1-naphthyl)-N'-(3-ethylphenyl)-N'-methylguanidine: a new, selective noncompetitive NMDA receptor antagonist.
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Diarylguanidines, acting as NMDA receptor ion channel site ligands, represent a new class of potential neuroprotective drugs. Several diarylguanidines structurally related to N,N'-di-o-tolylguanidine (DTG), a known selective sigma receptor ligand, were synthesized and evaluated in in vitro
New CNS-specific calcium antagonists.
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Ischemic insults to the brain in stroke or traumatic brain injury produce excessive release of glutamate from depolarized nerve terminals. This excessive glutamate release in turn stimulates massive calcium entry into nerve cells, activating a biochemical cascade that results in cell death. A major
Synthesis and pharmacological evaluation of N-(2,5-disubstituted phenyl)-N'-(3-substituted phenyl)-N'-methylguanidines as N-methyl-D-aspartate receptor ion-channel blockers.
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In the mammalian central nervous system, the N-methyl-D-aspartate (NMDA) subclass of glutamate receptors may play an important role in brain diseases such as stroke, brain or spinal cord trauma, epilepsy, and certain neurodegenerative diseases. Compounds which specifically antagonize the actions of
Neuroprotective use-dependent blockers of Na+ and Ca2+ channels controlling presynaptic release of glutamate.
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We have originated a family of N,N'-disubstituted guanidines that block the voltage-activated Ca2+ and Na+ channels governing glutamate release. These compounds, CNS 1237 (N-acenaphthyl-N'-methoxynaphthyl guanidine) and its analogues, are "use dependent" in their ability to attenaute
Heteroarylguanidines as Allosteric Modulators of ASIC1a and ASIC3 Channels.
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Acid-sensing ion channels (ASICs) are neuronal Na+-selective ion channels that open in response to extracellular acidification. They are involved in pain, fear, learning, and neurodegeneration after ischemic stroke. 2-Guanidine-4-methylquinazoline (GMQ) was recently discovered as the first nonproton
sigma-1 receptor modulation of acid-sensing ion channel a (ASIC1a) and ASIC1a-induced Ca2+ influx in rat cortical neurons.
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Acid-sensing ion channels (ASICs) are proton-gated cation channels found in peripheral and central nervous system neurons. The ASIC1a subtype, which has high Ca2+ permeability, is activated by ischemia-induced acidosis and contributes to the neuronal loss that accompanies ischemic stroke. Our
Left ventricular function in terminal uremia. A hemodynamic and echocardiographic study.
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14 patients with advanced uremia had a mean cardiac index (CI) of 4.37 +/- 0.25 liters/min/m2, a mean stroke work index (SWI) of 65.6 +/- 3.7 g/m/m2 and a mean left ventricular filling pressure (LVFP) of 16.3 +/- 2.1 mm Hg. The left ventricular performance was estimated to be normal when CI or SWI
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