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Titolo:
Protective role of nitric oxide in ischemia and reperfusion injury of the liver
Autore:
Shimamura, T; Zhu, Y; Zhang, SM; Jin, MB; Ishizaki, N; Urakami, A; Totsuka, E; Kishida, A; Lee, R; Subbotin, V; Furukawa, H; Starzl, TE; Todo, S;
Indirizzi:
Hokkaidopaniv, Sch Med, Dept Surg 1, Kita Ku, Sapporo, Hokkaido 0608638, Ja Hokkaido Univ Sapporo Hokkaido Japan 0608638 apporo, Hokkaido 0608638, Ja Univ Pittsburgh, Thomas E Starzl Transplantat Inst, Pittsburgh, PA USA Univ Pittsburgh Pittsburgh PA USA Transplantat Inst, Pittsburgh, PA USA
Titolo Testata:
JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS
fascicolo: 1, volume: 188, anno: 1999,
pagine: 43 - 52
SICI:
1072-7515(199901)188:1<43:PRONOI>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
L-ARGININE; MYOCARDIAL-ISCHEMIA; HEPATIC ISCHEMIA; BLOOD-PRESSURE; RAT-LIVER; ENDOTHELIUM; INHIBITION; FK409; CELLS; ISCHEMIA/REPERFUSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Todo, S Hokkaido608638,Sch Med, Dept Surg 1, Kita Ku, N-15,W-7, Sapporo, Hokkaido 0 Hokkaido Univ N-15,W-7 Sapporo Hokkaido Japan 0608638 , Hokkaido 0
Citazione:
T. Shimamura et al., "Protective role of nitric oxide in ischemia and reperfusion injury of the liver", J AM COLL S, 188(1), 1999, pp. 43-52

Abstract

Background: The suppressed production of nitric oxide (NO), associated with endothelial dysfunction, is thought to be a cause of ischemia and reperfusion injury of the liver. But findings of the salutary effects of NO enhancement on such injury have been conflicting. In this study, we tested our hypothesis that NO enhancement would attenuate ischemic liver injury. For this,purpose, an NO precursor, L-arginine, and a novel NO donor, FK409, were applied to a 2-hour total hepatic vascular exclusion model in dogs. Study Design: L-arginine was administered TV at a dose of 100 mg/kg twice (n = 5), while 300 mg/kg twice of FK409 was infused continuously into the portal vein (n = 5). The drugs were given to the animals for 30 and 60 minutes before and after ischemia, respectively. Nontreated animals were used asthe control (n = 10). Two-week survival, systemic and hepatic hemodynamicsindices, liver function tests, energy metabolism, and histopathology were analyzed. Results: Both treatments comparably augmented hepatic tissue blood flow decreased liver enzyme release, and increased high-energy phosphate restoration during the reperfusion period, all of which contributed to rescuing all of the treated animals from the 2-hour total hepatic ischemia. In contrast,ischemia caused 70% mortality in the control group. Histologically, structural abnormality and neutrophil infiltration were markedly attenuated by the treatments. Systemic hypotension was observed in the animals treated withFK409, however. Conclusions: Our data demonstrate that NO enhancement alleviates the liverinjury caused by ischemia and reperfusion. The supplementation of L-arginine, rather than FK409, is considered more applicable to clinical use because of the absence of systemic adverse effects. (J Am Coll Surg 1999;188:43-52. (C) 1999 by the American College of Surgeons).

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Documento generato il 04/04/20 alle ore 21:42:18