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Titolo:
Endothelin B receptor-mediated protection against anoxia-reoxygenation injury in perfused rat liver: Nitric oxide-dependent and -independent mechanisms
Autore:
Taniai, H; Suematsu, M; Suzuki, T; Norimizu, S; Hori, R; Ishimura, Y; Nimura, Y;
Indirizzi:
Keio Univ, Sch Med, Dept Biochem, Shinjuku Ku, Tokyo 1608582, Japan Keio Univ Tokyo Japan 1608582 Biochem, Shinjuku Ku, Tokyo 1608582, Japan Nagoya Univ, Sch Med, Dept Surg 1, Nagoya, Aichi 466, Japan Nagoya Univ Nagoya Aichi Japan 466 Dept Surg 1, Nagoya, Aichi 466, Japan
Titolo Testata:
HEPATOLOGY
fascicolo: 4, volume: 33, anno: 2001,
pagine: 894 - 901
SICI:
0270-9139(200104)33:4<894:EBRPAA>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
BILE-ACID SECRETION; CARBON-MONOXIDE; VESICULAR TRANSPORT; HEPATIC LIPOCYTES; ANTAGONIST; ISCHEMIA; CONTRACTION; TARGET; CELLS; VASOCONSTRICTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Suematsu, M Keio Univ, Sch Med, Dept Biochem, Shinjuku Ku, 35 Shinanomachi, Tokyo 1608582, Japan Keio Univ 35 Shinanomachi Tokyo Japan 1608582 1608582, Japan
Citazione:
H. Taniai et al., "Endothelin B receptor-mediated protection against anoxia-reoxygenation injury in perfused rat liver: Nitric oxide-dependent and -independent mechanisms", HEPATOLOGY, 33(4), 2001, pp. 894-901

Abstract

This study aimed to investigate the roles of endothelin (ET) receptors in biliary dysfunction and cell injury in postischemic livers. Rat livers perfused with oxygenated Krebs-Henseleit solution were exposed to reoxygenationfollowing 20-minute hypoxia. The anoxic perfusion decreased bile output and reduced cyclic guanosine monophosphate (cGMP) contents, an index of nitric oxide (NO) generation. Upon reoxygenation, the decreased bile was not fully recovered, and the resistance increased biphasically: an early transientspike accompanied by an elevated release of ET-1 and a rise accompanied bya cGMP elevation in the later period. The initial vasoconstriction appeared to be mediated by both ETA and ETB receptors, as judged by inhibitory effects of their antagonists, BQ-485 and BQ-788, respectively, while the late elevation of the resistance was not attenuated by these reagents, but rather enhanced by the ETB blockade. The BQ-788 treatment attenuated the reoxygenation-induced cGMP elevation and induced bile acid-dependent choleresis. However, such a change upon the ETB blockade coincided with dissociation of a recovery of phospholipids and aggravation of cell injury. The BQ-788-elicited deterioration of reoxygenation-elicited changes was attenuated by NO supplement with S-nitroso-N-acetyl penicillamine, N-w-Nitro-L-arginine methyl ester, an NO synthase inhibitor, mimicked biliary changes elicited by theETB blockade but without causing notable cell injury. Under these circumstances, coadministration of clotrimazole, an inhibitor of cytochrome P450 mono-oxygenases, elicited the injury comparable with that observed under the ETB blockade. These results suggest that ETB-mediated signaling limits excessive bile acid excretion and plays a protective role against reoxygenationinjury through mechanisms involving both NO-dependent an processes.

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Documento generato il 23/01/21 alle ore 08:32:55