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Titolo:
Molecular mechanisms in the early phase of hemorrhagic shock
Autore:
Hierholzer, C; Billiar, TR;
Indirizzi:
Tech Univ Munich, Klinikum Rechts Isar, Chirurg Klin, D-81675 Munich, Germany Tech Univ Munich Munich Germany D-81675 rg Klin, D-81675 Munich, Germany Univ Pittsburgh, Dept Surg, Pittsburgh, PA 15260 USA Univ Pittsburgh Pittsburgh PA USA 15260 pt Surg, Pittsburgh, PA 15260 USA
Titolo Testata:
LANGENBECKS ARCHIVES OF SURGERY
fascicolo: 4, volume: 386, anno: 2001,
pagine: 302 - 308
SICI:
1435-2443(200107)386:4<302:MMITEP>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; ISCHEMIA-REPERFUSION INJURY; HYPOXIA-INDUCIBLE FACTOR-1; BACTERIAL TRANSLOCATION; CELLS; NEUTROPHILS; STAT3; RATS; MICE; DECOMPENSATION;
Keywords:
hemorrhagic shock; inflammatory cascade; shock-dependent and reperfusion-dependent; mechanisms; inflammatory signaling;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Hierholzer, C Tech Univ Munich, Klinikum Rechts Isar, Chirurg Klin, Ismaningerstr 22, D-81675 Munich, Germany Tech Univ Munich Ismaningerstr 22 Munich Germany D-81675 ny
Citazione:
C. Hierholzer e T.R. Billiar, "Molecular mechanisms in the early phase of hemorrhagic shock", LANG ARCH S, 386(4), 2001, pp. 302-308

Abstract

Hemorrhagic shock (HS) results in the initiation of an inflammatory cascade that is critical for survival following successful resuscitation. We identified a complex sequence of molecular events including shock-dependent andreperfusion-dependent responses that offer a new comprehensive approach for consequences of HS. Shock-dependent initializing mechanisms include the induction of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX) -2, and CD14 and play a catalyzing role for subsequent phenotypic changes following resuscitation. The early immediate response genes iNOS and COX-2 promote the inflammatory response by the rapid and excessive production of nitric oxide (NO) and prostaglandins. The transcription factor hypoxia-inducible factor-1 (HIF-1) may regulate the induction of iNOS during the ischemic phase of shock. NO is an important signaling molecule which is involved in redox-sensitive mechanisms including the downstream activation of nuclear factor (NF)-kappaB. NO-dependent NF-kappaB activation promotes the inductionof inflammatory cytokine expression during the reperfusion phase. Peroxynitrite-mediated direct toxicity and NO-mediated inflammatory toxicity contribute: to organ injury. Patients suffering consequences of severe HS are susceptible to systemic inflammation, organ injury, and mortality if physiologic and therapeutic mechanisms are ineffective in limiting the activation ofthe inflammatory cascade.

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Documento generato il 18/01/20 alle ore 21:35:08