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Titolo:
Alpha-2 adrenergic receptor agonists are neuroprotective in experimental models of glaucoma
Autore:
Wheeler, LA; Woldemussie, E;
Indirizzi:
Allergan Pharmaceut Inc, Dept Biol Sci, Irvine, CA 92612 USA Allergan Pharmaceut Inc Irvine CA USA 92612 iol Sci, Irvine, CA 92612 USA
Titolo Testata:
EUROPEAN JOURNAL OF OPHTHALMOLOGY
, volume: 11, anno: 2001, supplemento:, 2
pagine: S30 - S35
SICI:
1120-6721(200107/09)11:<S30:AARAAN>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
GANGLION-CELL DEATH; INJURY; DEXMEDETOMIDINE; APOPTOSIS; ISCHEMIA; DAMAGE; RAT;
Keywords:
alpha-2 adrenoreceptor agonist; brimonidine; glaucoma; neuroprotection; neuroprotective signalling pathways;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Wheeler, LA Allergan Pharmaceut Inc, Dept Biol Sci, 2525 Dupont Dr, Irvine, CA 92612 USA Allergan Pharmaceut Inc 2525 Dupont Dr Irvine CA USA 92612 USA
Citazione:
L.A. Wheeler e E. Woldemussie, "Alpha-2 adrenergic receptor agonists are neuroprotective in experimental models of glaucoma", EUR J OPTHA, 11, 2001, pp. S30-S35

Abstract

PURPOSE. The glaucomas are characterized by chronic progressive ganglion cell loss over many years. A drug with neuroprotective activity should increase the resistance of retinal ganglion cells (RGC) to chronic stress or injury and therefore enhance survival. Brimonidine is a highly selective and potent alpha-2 adrenergic receptor agonist, which lowers intra-ocular pressure (IOP) and is neuroprotective. Immunohistochemistry data have shown that the specific receptor targets, the alpha-2 receptors, are located in the inner retina. METHODS. Brimonidine 0.1 mg/kg given intraperitoneally promoted RGC survival compared with vehicle using the optic nerve crush model even when administered up to 24 hours before injury. Using the chronic ocular hypertensive rat model, brimonidine 1 mg/kg/day (with osmotic pump) significantly prevented the loss of RGCs when compared with vehicle or timolol. This ability was due to the neuroprotective action of brimonidine, since it did not affectIOP. In addition, brimonidine 0.1 mg/day reached concentrations in the retina of Sprague-Dawley rats within 30 minutes of injection, which was sufficient to activate the alpha-2 receptor ( greater than or equal to 2 nM) and maintained these concentrations for 6 hours. CONCLUSIONS. Having demonstrated that:a. the specific receptor target of brimonidine is located in the retina, which is important for optic neuroprotection,b. the agent shows neuroprotective ability in animal models,c. pharmacological concentrations of the drug can be reached in the retina, clinical trial has been initiated to determine whether brimonidine is neuroprotective in patients with nonarteritic ischaemic optic neuropathy.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 23:47:01