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Titolo:
Basal release of nitric oxide and its interaction with endothelin-1 on single vessel hydraulis permeability
Autore:
Victorino, GP; Wisner, DH; Tucker, VL;
Indirizzi:
Univ Calif Davis, Hlth Syst, Dept Surg, Sacramento, CA 95817 USA Univ Calif Davis Sacramento CA USA 95817 t Surg, Sacramento, CA 95817 USA Univ Calif Davis, Dept Human Physiol, Sacramento, CA 95817 USA Univ Calif Davis Sacramento CA USA 95817 hysiol, Sacramento, CA 95817 USA
Titolo Testata:
JOURNAL OF TRAUMA-INJURY INFECTION AND CRITICAL CARE
fascicolo: 3, volume: 50, anno: 2001,
pagine: 535 - 539
Fonte:
ISI
Lingua:
ENG
Soggetto:
VENULAR PERMEABILITY; RELAXING FACTOR; CONSCIOUS RAT; RESPONSES; INVIVO;
Keywords:
capillary permeability; hydraulic conductivity; Landis technique; endothelin; nitric oxide; L-NAME;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Wisner, DH Univ Calif Davis, Hlth Syst, Dept Surg, 2315 Stockton Blvd,Room4209A, Sacramento, CA 95817 USA Univ Calif Davis 2315 Stockton Blvd,Room 4209A Sacramento CA USA 95817
Citazione:
G.P. Victorino et al., "Basal release of nitric oxide and its interaction with endothelin-1 on single vessel hydraulis permeability", J TRAUMA, 50(3), 2001, pp. 535-539

Abstract

Background: Both endothelin-l (ET-1) and nitric oxide (NO) are released bythe endothelium and are implicated in modulating the permeability of the endothelial barrier. The present study was designed to examine the interaction between ET-1 and NO and its influence on microvascular permeability as well as the role of NO in maintaining microvascular permeability. To isolatethe direct effect of ET-1 and NO, experiments were conducted under conditions where hydraulic and oncotic pressures were controlled. Methods: Postcapillary venules in the rat mesentery were perfused in situ and paired measurements of hydraulic permeability (L-p) obtained using the modified Landis micro-occlusion method. The effect of basal endogenous NO was tested by measuring the effects of perfusion with the NO synthase inhibitor N-w-nitro-L-arginine-methyl-ester (L-NAME) (100 mu mol/L) on L-p (n = 6), In addition, L-p measured after a 15-minute perfusion with L-NAME (100 mu mol/L) was compared with measures of L-p obtained after perfusion with a combined mixture of L-NAME (100 mu mol/L) and ET-1 (80 pmol/L) (n = 6). Results: Units for L-p are mean +/- SE x 10(-8) cm sec(-1) cm H2O-1. Underbasal conditions, in the absence of exogenous ET-1, NO synthase inhibitionled to a significant increase in L-p from 5.7 +/- 0.5 to 9.8 +/- 1.4 (p = 0,02), Compared with L- NAME alone, ET-1 + L-NAME significantly decreased L-p from 10.3 +/- 0.8 to 5.7 +/- 0.6 (p = 0,006),Conclusion: Constitutive release of NO from the microvascular endothelium plays a role in maintaining a basal level of microvascular permeability, Decreases in microvascular permeability seen with the administration of ET-1 are not mediated via the release of NO. These findings suggest important roles for ET-1 and NO in maintaining and modulating microvascular permeability.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/08/20 alle ore 20:52:33