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Titolo:
Nitric oxide synthetase activity in cerebral post-ischemic reperfusion andeffects of L-N-G-Nitroarginine and 7-nitroindazole on the survival
Autore:
Sorrenti, V; Di Giacomo, C; Campisi, A; Perez-Polo, JR; Vanella, A;
Indirizzi:
Univ Catania, Inst Biol Chem, Catania, Italy Univ Catania Catania ItalyUniv Catania, Inst Biol Chem, Catania, Italy Univ Texas, Med Branch, Dept Human Biol Chem & Genet, Galveston, TX 77550 USA Univ Texas Galveston TX USA 77550 l Chem & Genet, Galveston, TX 77550 USA
Titolo Testata:
NEUROCHEMICAL RESEARCH
fascicolo: 7, volume: 24, anno: 1999,
pagine: 861 - 866
SICI:
0364-3190(199907)24:7<861:NOSAIC>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSTISCHEMIC REPERFUSION; LIPID-PEROXIDATION; 7-NITRO INDAZOLE; INFARCT VOLUME; NERVOUS-SYSTEM; RAT MODEL; SYNTHASE; INHIBITION; GLUTAMATE; CEREBELLUM;
Keywords:
NOS; cerebral ischemia; 7-NI; L-N-G-NA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Vanella, A Univ Catania, Prof Angelo Vanella Inst Biochem, Vle A Doria 6, I-95125 Catania, Italy Univ Catania Vle A Doria 6 Catania Italy I-95125 atania, Italy
Citazione:
V. Sorrenti et al., "Nitric oxide synthetase activity in cerebral post-ischemic reperfusion andeffects of L-N-G-Nitroarginine and 7-nitroindazole on the survival", NEUROCHEM R, 24(7), 1999, pp. 861-866

Abstract

Nitric Oxide (NO) mediates a series of physiological processes including regulation of vascular tone, macrophage-mediated cytotoxicity, platelet aggregation, learning and long-term potentiation, neuronal transmission. Although NO mediates several physiological functions, overproduction of NO can bedetrimental and play multiple roles in the pathophysiology of focal cerebral ischemia. In the present study NOS activities were evaluated in cerebellum and cerebral cortex of ischemic and post-ischemic reperfused rats using an experimental model of partial cerebral ischemia; moreover, the effects of L-N(G)Nitroarginine (NA, nonselective NOS inhibitor) or 7-Nitroindazole (7-NI, selective neuronal NOS inhibitor) administration were assayed on percentage survival of ischemic rats. An increase of NOS activity in the cerebellum and in cerebral cortex of ischemic and post-ischemic reperfused rats was observed. NA administration failed to induce neuroprotective effects, byincreasing percentage of mortality of treated ischemic rats with respect to control group. In contrast, the treatment with the selective neuronal NOSinhibitor, 7-NI, induced a significant neuroprotective effect.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 03:31:38