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Titolo:
NITRIC-OXIDE AND PROSTAGLANDIN E-2 FORMATION PARALLELS BLOOD-BRAIN-BARRIER DISRUPTION IN AN EXPERIMENTAL RAT MODEL OF BACTERIAL-MENINGITIS
Autore:
JAWOROWICZ DJ; KORYTKO PJ; LAKHMAN SS; BOJE KMK;
Indirizzi:
UNIV BUFFALO,DEPT PHC,H517 COOKE HOCHSTETTER BUFFALO NY 14260 UNIV BUFFALO,SCH PHARM,DEPT PHARMACEUT BUFFALO NY 00000
Titolo Testata:
Brain research bulletin
fascicolo: 6, volume: 46, anno: 1998,
pagine: 541 - 546
SICI:
0361-9230(1998)46:6<541:NAPEFP>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; EXPERIMENTAL PNEUMOCOCCAL MENINGITIS; NITROGEN-OXIDES; TNF-ALPHA; SYNTHASE; PATHOPHYSIOLOGY; PERMEABILITY; INJURY; CYCLOOXYGENASE; INTERLEUKIN-1;
Keywords:
NITRIC OXIDE; PROSTAGLANDIN E-2; MENINGITIS; BLOOD-BRAIN BARRIER; PERMEABILITY KINETICS; LIPOPOLYSACCHARIDES; INFLAMMATORY MEDIATORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
44
Recensione:
Indirizzi per estratti:
Citazione:
D.J. Jaworowicz et al., "NITRIC-OXIDE AND PROSTAGLANDIN E-2 FORMATION PARALLELS BLOOD-BRAIN-BARRIER DISRUPTION IN AN EXPERIMENTAL RAT MODEL OF BACTERIAL-MENINGITIS", Brain research bulletin, 46(6), 1998, pp. 541-546

Abstract

During meningitis, the host produces a plethora of signaling agents as part of a coordinated defense mechanism against invading pathogens. Nitric oxide (NO) and prostaglandin E-2 (PGE(2)) are two such inflammatory mediators produced in response to bacterial endotoxins. Disruption of the blood-brain barrier (BBB) is one of many pathophysiological consequences of meningitis. The present objective was to examine the timecourse of NO and PGE, production in relationship to BBB permeabilityalterations during experimentally-induced meningitis. Meningeal inflammation was elicited by intracisternal administration of the bacterialendotoxin, lipopolysaccharides (LPS; 200 mu g), and NO, PGE(2), and BBB integrity were monitored over the next 24 h. Meningeal NO production was assessed by headspace chemiluminescence; cerebrospinal fluid PGE(2) was determined by enzyme-linked immunosorbent assay (ELISA) immunoassay; and BBB integrity was determined by the brain accumulation of C-14-sucrose. Similar time-course profiles for NO and PGE(2) were observed, with a peak effect for both inflammatory mediators observed within 6-8 h after intracisternal LPS dosing. Statistically significant (p < 0.05) disruption of the BBB was observed in various brain regions. Strikingly similar temporal relationships were observed for NO and PGE(2) production and BBB disruption. These results suggest the hypothesisthat NO and PGE(2) may act in conjunction to disrupt the BBB during experimental meningitis. (C) 1998 Elsevier Science Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 15:10:14