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Titolo:
Prolonged suppression of brain nitric oxide synthase activity by 7-nitroindazole protects against cerebral hypoxic-ischemic injury in neonatal rat
Autore:
Ishida, A; Trescher, WH; Lange, MS; Johnston, MV;
Indirizzi:
Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 Neurol, Baltimore, MD 21205 USA Kennedy Krieger Res Inst, Baltimore, MD 21205 USA Kennedy Krieger Res Inst Baltimore MD USA 21205 , Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 Pediat, Baltimore, MD 21205 USA
Titolo Testata:
BRAIN & DEVELOPMENT
fascicolo: 5, volume: 23, anno: 2001,
pagine: 349 - 354
SICI:
0387-7604(200108)23:5<349:PSOBNO>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
HYPOTHERMIC CIRCULATORY ARREST; NEURONAL NADPH DIAPHORASE; 7-NITRO INDAZOLE; INFARCT VOLUME; IN-VIVO; FOREBRAIN ISCHEMIA; MONOAMINE-OXIDASE; ARTERY OCCLUSION; NOS INHIBITOR; MODEL;
Keywords:
cerebral ischemia; newborn; nitric oxide synthase; N-methyl-D-aspartate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
59
Recensione:
Indirizzi per estratti:
Indirizzo: Trescher, WH Johns Hopkins Univ, Sch Med, Dept Neurol, 707 N Broadway, Baltimore, MD 21205 USA Johns Hopkins Univ 707 N Broadway Baltimore MD USA 21205 USA
Citazione:
A. Ishida et al., "Prolonged suppression of brain nitric oxide synthase activity by 7-nitroindazole protects against cerebral hypoxic-ischemic injury in neonatal rat", BRAIN DEVEL, 23(5), 2001, pp. 349-354

Abstract

Nitric oxide mediates glutamate-induced excitotoxicity associated with cerebral hypoxia-ischemia through production in the brain by several isoforms of nitric oxide synthase NOS). We examined the influence of the selective neuronal NOS inhibitor, 7-nitroindazole (7-NI), on brain NOS activity and its neuroprotective effects against cerebral hypoxic-ischemic injury in the postnatal day (PND) 7 rat. In the first set of experiments, 7-NI (50 mg/kg) administered intrapetitoneally (i.p.) transiently inhibited NOS activity to40% below the vehicle control level at 1h after injection (P < 0.001, analysis of variance (ANOVA)). In contrast, 7-NI (100 mg/kg, i.p.) inhibited NOS activity to 56% below the control level at I It with prolonged suppression of NOS activity at 3, 6, 9 and 12 h after injection. Two-factor ANOVA revealed an overall effect on NOS activity of 7-NI treatment (P < 0.001) and time after injection (P < 0.001). In the second set of experiments, 7-NI 50,100 mg/kg) or an equal volume of vehicle was administered after unilateralcarotid artery ligation, but 30 min before hypoxia in PND 7 rats. 7-NI (100 mg/kg) significantly protected against cerebral hypoxic-ischemic injury (100 mg/kg of 7-NI, 1.7 1.0% damage; control, 8.7 1.6%,P < 0.05). 7-NI administered 15 min after cerebral hypoxia-ischemia was not neuroprotective. Thedata suggest that the protective effect of 7-NI is dose dependent, and is related to the duration of suppressed NOS activity. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 17:56:17