Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0600097 (Sedation)
 1,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During cerebral ischaemia, glutamate is released in supraphysiological amounts and is toxic to brain tissue. This excitotoxicity is mediated by several glutamate receptor subtypes, including the ionotropic N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors. Clinical trials of drugs that block the NMDA receptor in acute ischaemic stroke have been disappointing. No improvement in clinical outcome of stroke has been seen with competitive NMDA antagonists (selfotel) and non-competitive NMDA antagonists (dextrorphan, GV150526, aptiganel and eliprodil). The AMPA receptor differs in important ways from the NMDA receptor. It is the principal mediator of fast excitatory neurotransmission. This ligand-gated cation channel is primarily permeable to sodium rather than calcium. It is found in grey and white matter. It is expressed by oligodendrocytes. This distribution may provide neuroprotection for both grey and white matter. In a variety of animal models, reduction in infarct volume with AMPA blockade has been demonstrated. AMPA antagonists also show benefit in spinal cord ischaemia and trauma. The clinical development of safe and effective AMPA blockers has been hampered by poor water solubility and associated renal toxicity. A novel, highly water-soluble, competitive AMPA receptor antagonist, YM872 ([2,3-dioxo-7-(1H-imidazol-1-yl)-6-nitro-1,2,3,4-tetrahydroquinoxalin-1-yl]acetic acid monohydrate; Yamanouchi), has been identified. Phase I clinical trial data indicate that this agent can be safely administered in young and elderly subjects. Sedation and other CNS associated adverse events determine the ceiling dose and become more problematic with infusion times exceeding 24 h. Phase II studies of YM872 in acute ischaemic stroke are ongoing.
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PMID:Glutamate AMPA receptor antagonist treatment for ischaemic stroke. 1236 32

Fran The effects of sedation and of halogenate anesthesia on electroretinographic recordings were investigated by reviewing the hospital charts of 27 patients who were eventually diagnosed free of retinal disease. The same ERG protocol was performed in conscious (n=9), sedated (chloral hydrate or pentobarbital sodium, n=9) and anesthetized (halothane or isoflurane, in combination with N2O, n=9) young patients. Sedation decreased the a- and b-wave amplitude of the scotopic bright-flash response, without affecting implicit times. ERG recordings performed in photopic conditions showed minimal disturbances. Anesthesia spared the a-wave of the scotopic bright-flash response but decreased more severely the b-wave. In addition, anesthesia reduced the amplitude and prolonged the implicit time of the photopic responses, affecting predominantly the ionotropic glutamate dependent OFF components (peak of b-wave, 0P4 and 0P5). The normal retinal physiology is affected by sedation and anesthesia through different mechanisms that still remain to be fully elucidated. These alterations in electroretinographic recordings must be considered when evaluating ERGs obtained under similar sedation/anesthetized conditions.
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PMID:Alteration of electroretinographic recordings when performed under sedation or halogenate anesthesia in a pediatric population. 1471 Nov 59