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Titolo:
Altered release of prostaglandins contributes to hypoxic/ischemic impairment of NOC/oFQ cerebrovasodilation
Autore:
Armstead, WM;
Indirizzi:
Univ Penn, Dept Anesthesia, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 nesthesia, Philadelphia, PA 19104 USA Univ Penn, Dept Pharmacol, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Pharmacol, Philadelphia, PA 19104 USA
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1, volume: 859, anno: 2000,
pagine: 104 - 112
SICI:
0006-8993(20000317)859:1<104:AROPCT>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
OPIOID RECEPTOR FAMILY; NEWBORN PIG BRAIN; REGIONAL DISTRIBUTION; ARTERIOLAR DILATION; TISSUE DISTRIBUTION; VASCULAR-RESPONSES; MOLECULAR-CLONING; ORL1 RECEPTOR; GENE FAMILY; ISCHEMIA;
Keywords:
newborn; cerebral circulation; opioid; cerebral ischemia; prostaglandin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Armstead, WM Univ Penn, Dept Anesthesia, 3400 Spruce St, Philadelphia, PA 19104 USA Univ Penn 3400 Spruce St Philadelphia PA USA 19104 19104 USA
Citazione:
W.M. Armstead, "Altered release of prostaglandins contributes to hypoxic/ischemic impairment of NOC/oFQ cerebrovasodilation", BRAIN RES, 859(1), 2000, pp. 104-112

Abstract

This study was designed to determine if altered release of prostaglandins contributes to impaired pi:ll artery dilation to the newly described opioid, nociceptin/orphanin FQ (NOC/oFQ), following hypoxia/ischemia in newborn pigs equipped with a closed cranial window. Global cerebral ischemia (20 min) was induced via elevation of intracranial pressure, while hypoxia (10 min) decreased P-O2 to 35 +/- 3 mmHg with unchanged P-CO2. NOC/oFQ (10(-8) and10(-6) M) modestly increased cerebrospinal fluid (CSF) 6-Keto PGF(1 alpha)and TXB2, the stable breakdown products of PGI(2) and TXA(2), in sham animals (1199 +/- 39 to 1704 +/- 104 and 299 +/- 9 to 409 +/- 12 pg/ml for control and 10(-6) M NOC/oFQ 6-Keto PGF(1 alpha) and TXB2, respectively). In 1 h post ischemia/reperfusion (I + R) animals, basal levels of 6-Keto PGF(1 alpha) and TXB2 were elevated. NOC/oFQ-stimulated release of 6-Keto PGF(1 alpha) was blocked while such release of TXB2 was enhanced (526 +/- 15 to 822+/- 36 pg/ml for control and 10(-6) M NOC/oFQ CSF TXB2). Similar, though more pronounced, changes were observed in hypoxia/ischemia/reperfusion (H + I + R) animals. Pretreatment with indomethacin (5 mg/kg i.v.) or SQ 29.548 (10(-4) M), cyclooxygenase and PGH(2)/TXA(2) receptor antagonists, partially restored attenuated NOC/oFQ pial artery dilation 1 h after I + R (9 +/- 1and 18 +/- 1 vs. 3 +/- 1 and 6 +/- 1 vs. 8 +/- 1 and 13 +/- 1% for 10(-8) and 10(-6) M NOC/oFQ in sham, I + R, and I + R - SQ 29,548 pretreated animals). In contrast, NOC/oFQ-induced vasodilation was reversed to vasoconstriction in H + I + R animals and indomethacin or SQ 29,548 similarly partiallyrestored such pial vasodilation. These data indicate that altered stimulated prostaglandin release contributes to hypoxic/ischemic impairment of NOC/oFQ-mediated pial artery dilation. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 11:38:46