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Titolo:
The effects of nitric oxide on shock caused by temporary hepatic inflow occlusion in pigs
Autore:
Saito, A; Ohwada, S; Ikeda, T; Matsuno, N; Kozaki, M;
Indirizzi:
Gunma Univ, Sch Med, Dept Surg 2, Maebashi, Gumma 371, Japan Gunma Univ Maebashi Gumma Japan 371 pt Surg 2, Maebashi, Gumma 371, Japan Tokyo Med Coll, Dept Anesthesiol, Hachioji Med Ctr, Tokyo 160, Japan TokyoMed Coll Tokyo Japan 160 esiol, Hachioji Med Ctr, Tokyo 160, Japan Tokyo Med Coll, Dept Surg 5, Hachioji Med Ctr, Tokyo 160, Japan Tokyo Med Coll Tokyo Japan 160 urg 5, Hachioji Med Ctr, Tokyo 160, Japan
Titolo Testata:
HEPATO-GASTROENTEROLOGY
fascicolo: 25, volume: 46, anno: 1999,
pagine: 436 - 442
SICI:
0172-6390(199901/02)46:25<436:TEONOO>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
ARGININE METHYL-ESTER; ANAPHYLACTIC SHOCK; HEMODYNAMICS; PERMEABILITY; DYSFUNCTION; REPERFUSION; ADHESION;
Keywords:
NO; L-NAME; L-arginine; shock; hepatic inflow occlusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Saito, A Gunma Univ, Sch Med, Dept Surg 2, 3-39-15 Showa Machi, Maebashi, Gumma 371, Gunma Univ 3-39-15 Showa Machi Maebashi Gumma Japan 371 umma 371,
Citazione:
A. Saito et al., "The effects of nitric oxide on shock caused by temporary hepatic inflow occlusion in pigs", HEP-GASTRO, 46(25), 1999, pp. 436-442

Abstract

BACKGROUND/AIMS: Nitric oxide (NO) plays an important role in the regulation of systemic hemodynamics in various shock status. The effect of NO on shock induced by hepatic inflow occlusion has not been previously investigated. METHODOLOGY: We examined the effects of NO on systemic hemodynamics and oxygen metabolism in shock caused by temporary hepatic inflow occlusion without bypass in pigs using NO synthase inhibitor, N-G-nitro-L-arginine methyl ester (NAME group) and the substrate for NO synthesis, L-arginine (ARG group). RESULTS: All animals in the control and ARG group tolerated the surgery, while 2 of 5 animals in the NAME group died during the occlusion period. Cardiac output and mixed venous oxygen saturation (SvO2) in the NAME group wassignificantly reduced compared with the other two groups during and after hepatic inflow occlusion. In contrast, SvO2 in the ARG group was maintainedat higher levels throughout the study period, and the recovery time of cardiac output following reperfusion was earlier than that of the other two groups. CONCLUSIONS: Endogenous NO inhibition exacerbates the shock status inducedby hepatic inflow occlusion. Exogenous administration of NO donor may improve the shock status induced by hepatic inflow occlusion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/10/20 alle ore 05:20:36