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Titolo:
Enhanced post-ischemic liver injury in iNOS-deficient mice: A cautionary note
Autore:
Hines, IN; Harada, H; Bharwani, S; Pavlick, KP; Hoffman, JM; Grisham, MB;
Indirizzi:
Louisiana State Univ, Hlth Sci Ctr, Dept Mol & Cellular Physiol, Shreveport, LA 71130 USA Louisiana State Univ Shreveport LA USA 71130 ol, Shreveport, LA 71130 USA
Titolo Testata:
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
fascicolo: 4, volume: 284, anno: 2001,
pagine: 972 - 976
SICI:
0006-291X(20010622)284:4<972:EPLIII>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; MICROVASCULAR BLOOD-FLOW; REPERFUSION INJURY; ISCHEMIA/REPERFUSION INJURY; HEPATIC ISCHEMIA; RAT-LIVER; INHIBITION; ENDOTOXEMIA; ACTIVATION; CYTOKINES;
Keywords:
neutrophils; inflammation; transplantation; microcirculation; free radicals;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Grisham, MB Louisiana State Univ, Hlth Sci Ctr, Dept Mol & Cellular Physiol, 1501 Kings Highway, Shreveport, LA 71130 USA Louisiana State Univ 1501 Kings Highway Shreveport LA USA 71130
Citazione:
I.N. Hines et al., "Enhanced post-ischemic liver injury in iNOS-deficient mice: A cautionary note", BIOC BIOP R, 284(4), 2001, pp. 972-976

Abstract

The objective of this study was to assess the role of inducible nitric oxide synthase (iNOS) in ischemia and reperfusion (I/R)-induced liver injury, We found that partial hepatic ischemia involving 70% of the liver resulted in a time-dependent increase in serum alanine aminotransferase (ALT) levelsat 1-6 h following reperfusion. Liver injury at 1, 3, and 6 h post-ischemia was not due to the infiltration of neutrophils as assessed by tissue myeloperoxidase (MPO) activity and histopathology. iNOS-deficient mice subjected to the same duration of ischemia and reperfusion showed dramatic and significant increases in liver injury at 3 but not 6 h following reperfusion compared to their wild type controls. Paradoxically, iNOS mRNA expression wasnot detected in the livers of wild type mice at any point during the reperfusion period and pharmacological inhibition of iNOS using L-N-6(iminoethyl)-lysine (L-NIL) did not exacerbate post-ischemic liver injury at any time post-reperfusion. These data suggest that iNOS deficiency produces unanticipated genetic alterations that renders these mice more sensitive to liver I/R-induced injury. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 15:30:34