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Titolo:
Fetal cerebral and peripheral circulatory responses to hypoxia after nitric oxide synthase inhibition
Autore:
Harris, AP; Helou, S; Gleason, CA; Traystman, RJ; Koehler, RC;
Indirizzi:
Johns Hopkins Med Inst, Dept Anesthesiol & Crit Care Med, Baltimore, MD 21287 USA Johns Hopkins Med Inst Baltimore MD USA 21287 ed, Baltimore, MD 21287 USA Johns Hopkins Med Inst, Dept Pediat, Baltimore, MD 21287 USA Johns HopkinsMed Inst Baltimore MD USA 21287 at, Baltimore, MD 21287 USA Univ Washington, Dept Pediat, Seattle, WA 98195 USA Univ Washington Seattle WA USA 98195 , Dept Pediat, Seattle, WA 98195 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY
fascicolo: 2, volume: 281, anno: 2001,
pagine: R381 - R390
SICI:
0363-6119(200108)281:2<R381:FCAPCR>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-FLOW; SYMPATHETIC VASOCONSTRICTION; INTRACRANIAL HYPERTENSION; OXYGEN-METABOLISM; OVINE FETUS; SHEEP; LAMB; BRAIN; REACTIVITY; HYPOXEMIA;
Keywords:
cerebral blood flow; coronary blood flow; fetus; gastrointestinal blood flow; sheep;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
40
Recensione:
Indirizzi per estratti:
Indirizzo: Koehler, RC Johns Hopkins Med Inst, Dept Anesthesiol & Crit Care Med, 600 N Wolfe St Blalock 1404-E, Baltimore, MD 21287 USA Johns Hopkins Med Inst 600 N Wolfe St Blalock 1404-E Baltimore MD USA 21287
Citazione:
A.P. Harris et al., "Fetal cerebral and peripheral circulatory responses to hypoxia after nitric oxide synthase inhibition", AM J P-REG, 281(2), 2001, pp. R381-R390

Abstract

The increase in cerebral blood flow (CBF) during hypoxia in fetal sheep at0.6 gestation is less than the increase at 0.9 gestation when normalized for differences in baseline CBF and oxygen consumption. Nitric oxide (NO) synthase (NOS) catalytic activity increases threefold during this period of development. We tested the hypothesis that administration of the NOS inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) decreases the CBF response to systemic hypoxia selectively at 0.9 gestation. We also tested whether any peripheral vasoconstriction during hypoxia is potentiated by L-NAME at 0.9 gestation. Administration of L-NAME increased arterial blood pressure and decreased microsphere-determined CBF during normoxia in fetal sheep at both 0.6 and 0.9 gestation. With subsequent reduction of arterial oxygen content by similar to 50%, the percent increase in forebrain CBF in a control group (57 +/- 11%; +/- SE) and L-NAME-treated group (51 +/- 6%) was similarat 0.6 gestation. Likewise, at 0.9 gestation, the increase in CBF was similar in control (90 +/- 25%) and L-NAME (80 +/- 28%) groups. At 0.9 gestation, L-NAME treatment attenuated the increase in coronary blood flow and increased gastrointestinal vascular resistance during hypoxia. We conclude thatNO exerts a basal vasodilatory influence in brain as early as 0.6 gestation in fetal sheep but is not an important mechanism for hypoxic vasodilationin brain at either 0.6 or 0.9 gestation. Thus the developmental increase in NOS catalytic capacity does not appear to be responsible for developmental increases in the CBF response to hypoxia during this period. In contrast,NO modulates the vascular response to hypoxia in heart and gastrointestinal tract.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 11:42:49