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Titolo:
Nitric oxide redox species exert differential permeability effects on the blood-brain barrier
Autore:
Boje, KMK; Lakhman, SS;
Indirizzi:
SUNY Buffalo, Sch Pharm, Dept Pharmaceut, Buffalo, NY 14260 USA SUNY Buffalo Buffalo NY USA 14260 Dept Pharmaceut, Buffalo, NY 14260 USA
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 2, volume: 293, anno: 2000,
pagine: 545 - 550
SICI:
0022-3565(200005)293:2<545:NORSED>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXPERIMENTAL MENINGITIS; CEREBROSPINAL-FLUID; INTRACRANIAL-PRESSURE; PERFUSION TECHNIQUE; MULTIPLE-SCLEROSIS; SYNTHASE; RAT; DISEASES; MICROCIRCULATION; PATHOGENESIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Boje, KMK SUNY Buffalo, Sch Pharm, Dept Pharmaceut, H517 Cooke Hochstetter, Buffalo,NY 14260 USA SUNY Buffalo H517 Cooke Hochstetter Buffalo NY USA 14260 260 USA
Citazione:
K.M.K. Boje e S.S. Lakhman, "Nitric oxide redox species exert differential permeability effects on the blood-brain barrier", J PHARM EXP, 293(2), 2000, pp. 545-550

Abstract

Excessive production of nitric oxide (NO) in the central nervous system issuspected to contribute to neurodegenerative diseases. Previous studies showed that excessive central nervous system NO increased the permeability ofthe blood-brain barrier (BBB) during experimental meningitis. The present work hypothesizes that the various NO redox forms (NO., NO+, NO-) differentially mediate disruption of the BBB. Pharmacological agents that release NOredox forms (i.e., NO prodrugs) were selected based on the rate of NO release and the liberated NO redox form. An in situ rodent brain perfusion preparation was used to administer NO prodrugs into the cerebrovascular circulation, followed by brain perfusion with [C-14]sucrose, a marker of BBB integrity. Cerebrovasculature infusion of certain NO prodrugs caused a significant, 2- to 5-fold BBB permeability increase in all forebrain regions (P < .01). The NO prodrug rank order of BBB disruption was S-nitroso-N-acetylpenicillamine-beta-cyclodextrin (releases NO., NO+, and NO-). Angeli's salt (NO., NO-) > MAHMA NONOate similar to diethylamine NONOate (NO.) > spermine NONOate (NO.) > DETA NONOate similar to Piloty's acid (negligible NO redox release); saline. When normalized to BBB disruption caused by hyperosmotic mannitol (100%), S-nitroso-N-acetylpenicillamine-beta-cyclodextrin (NO., NO+, and NO-) elicited similar to 45% disruption, Angeli's salt (NO., NO-) elicited similar to 18% disruption, and the NONOates (NO.) ranged from similar to 0 to 8% disruption. Cerebral blood flows and intracranial pressures were within normal limits for each tested NO prodrug, thereby suggesting that BBB disruption was not secondary to altered cerebral perfusion. Collectively,the results of this work identify that NO. alone exerts modest BBB disruption compared with the specie combination of NO. and NO-, and the greatest disruption is exerted by the combination of NO., NO-, and NO+.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 15:05:04