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adenosine/accidente cerebrovascular
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Adenosine kinase determines the degree of brain injury after ischemic stroke in mice.
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Adenosine kinase (ADK) is the major negative metabolic regulator of the endogenous neuroprotectant and homeostatic bioenergetic network regulator adenosine. We used three independent experimental approaches to determine the role of ADK as a molecular target for predicting the brain's susceptibility
European Stroke Prevention Study-2 results: serendipitous demonstration of neuroprotection induced by endogenous adenosine accumulation?
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In patients with prior stroke or transient ischaemic attack, anti-platelet treatment with dipyridamole substantially reduced stroke recurrence, with a beneficial effect comparable to and additive with that induced by aspirin (the European Stroke Prevention Study-2). Eugenio Picano and Maria
Adenosine, an identified active component from the Driselase-treated fraction of rice bran, is effective at improving metabolic syndrome in stroke-prone spontaneously hypertensive rats.
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In the present study, we isolated and identified an active component from the Driselase-treated fraction and investigated its effect by acute and chronic oral administration on hypertension, lipid, and glucose metabolism in stroke-prone spontaneously hypertensive rats. The active component was
Measurement of cardiac index and stroke volume using electrical cardiometry before and after administration of adenosine in a 6-year-old patient with supraventricular tachycardia.
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We report the case of a 6-year-old boy who developed a supraventricular tachycardia during an upper endoscopy while under general anesthesia. A noninvasive electrical cardiometry device was applied to the patient, and cardiac index and stroke volume were measured before and after the administration
Anti-metabolic syndrome effects of adenosine ingestion in stroke-prone spontaneously hypertensive rats fed a high-fat diet.
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We have demonstrated previously that both acute and chronic oral administration of adenosine have novel functions such as anti-hypertensive effects and improved hyperlipidaemia in stroke-prone spontaneously hypertensive rats (SHRSP) fed a normal diet. The purpose of the present study was to
Adenosine in the treatment of stroke: yes, maybe, or absolutely not?
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Agonist stimulation of adenosine A(1) receptors has been consistently shown to result in reduction of brain damage following experimentally induced global and focal brain ischaemia in animals. Unsurprisingly, the use of adenosine A(1) receptors as targets for the development of clinical therapeutics
[Minocycline Prevent Microglial Activation via Suppression of Adenosine A 2A Receptor in a Rat Stroke Ischemia/Reperfusion Model].
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OBJECTIVE
To investigate whether minocycline could inhibit neuroinflammation induced by microglia activation through suppression of adenosine A2Areceptor (A2AR)expression in rats after cerebral ischemia/reperfusion (I/R) injury.
METHODS
Thirty male Sprageue-Dawley rats were randomly divided into 3
Risk of stroke in patients with high on-clopidogrel platelet reactivity to adenosine diphosphate after percutaneous coronary intervention.
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Several prospective studies have shown that high on-clopidogrel platelet reactivity (HPR) in patients undergoing percutaneous coronary intervention (PCI) is a risk factor for ischemic events. All studies were insufficiently powered to detect differences in stroke between patients with HPR and those
Adenosine monophosphate activated protein kinase inhibition is protective in both sexes after experimental stroke.
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Sex differences in clinical and experimental stroke are now well recognized. Adenosine monophosphate activated protein kinase (AMPK) is an important energy sensor that is activated in times of energy demand. Increasing AMPK is deleterious in experimental cerebral ischemia, at least in males.
Novel effect of adenosine 5'-monophosphate on ameliorating hypertension and the metabolism of lipids and glucose in stroke-prone spontaneously hypertensive rats.
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The aim of the study was to investigate the effects of adenosine 5'-monophosphate (AMP) in stroke-prone spontaneously hypertensive rats (SHRSP). Male rats (10 weeks old) were divided into three groups: a control group fed an AIN-93 M diet and two others fed supplemental AMP (17.5 and 87.5 mg/kg
Adenosine diphosphate-induced platelet aggregation might contribute to poor outcomes in atrial fibrillation-related ischemic stroke.
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Systemic atherosclerosis is involved in ischemic damages and cardioembolism after atrial fibrillation (AF)-related ischemic stroke (IS). Platelet activation is a critical factor in systemic atherosclerosis; however, there is little information regarding the role of platelet activation on the outcome
Adenosine kinase, epilepsy and stroke: mechanisms and therapies.
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Adenosine is an inhibitory modulator of brain activity with neuroprotective and anticonvulsant properties. Adenosine levels are regulated mainly by adenosine kinase (ADK), an enzyme that is responsible for the removal of adenosine via phosphorylation to AMP. Recent evidence indicates that expression
Stroke as Initial Manifestation of Adenosine Deaminase 2 Deficiency.
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Deficiency of adenosine deaminase 2 (ADA2) due to homozygous or compound heterozygous mutations in the cat eye syndrome chromosome region, candidate 1 (CECR1) gene causes an autoimmune phenotype with systemic vasculitis affecting the skin, inner organs, and the central nervous system. Typically,
Increase in plasma adenosine during brain ischemia in man: a study during transient ischemic attacks, and stroke.
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Adenosine is a "retaliatory metabolite" which accumulates during experimental brain ischemia and has vasodilatory and putative neuroprotective effects. The aim of this study was to assess whether human cerebral ischemia and necrosis-evaluated in the clinical models of transient ischemic attack (TIA)
Adenosine and stroke: maximizing the therapeutic potential of adenosine as a prophylactic and acute neuroprotectant.
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Stroke is a leading cause of morbidity and mortality in the United States. Despite intensive research into the development of treatments that lessen the severity of cerebrovascular injury, no major therapies exist. Though the potential use of adenosine as a neuroprotective agent in the context of
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