PMID- 11466573
OWN - NLM
STAT- MEDLINE
DCOM- 20011101
LR  - 20200401
IS  - 1435-2443 (Print)
IS  - 1435-2451 (Electronic)
IS  - 1435-2443 (Linking)
VI  - 386
IP  - 4
DP  - 2001 Jul
TI  - Molecular mechanisms in the early phase of hemorrhagic shock.
PG  - 302-8
AB  - 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 and 
      reperfusion-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 induction of 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 of the inflammatory cascade.
FAU - Hierholzer, C
AU  - Hierholzer C
AD  - Chirurgische Klinik der Technischen Universitat Munchen, Klinikum Rechts der 
      Isar, Ismaningerstr. 22, 81675 Munchen. hierholzer@nt1.chir.med.tu-muenchen.de
FAU - Billiar, T R
AU  - Billiar TR
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Germany
TA  - Langenbecks Arch Surg
JT  - Langenbeck's archives of surgery
JID - 9808285
RN  - 0 (Cytokines)
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (HIF1A protein, human)
RN  - 0 (Hypoxia-Inducible Factor 1)
RN  - 0 (Hypoxia-Inducible Factor 1, alpha Subunit)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (Nuclear Proteins)
RN  - 0 (Transcription Factors)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.99.1 (Prostaglandin-Endoperoxide Synthases)
SB  - IM
MH  - Cytokines/metabolism
MH  - DNA-Binding Proteins/metabolism
MH  - Humans
MH  - Hypoxia-Inducible Factor 1
MH  - Hypoxia-Inducible Factor 1, alpha Subunit
MH  - Inflammation/metabolism/*physiopathology
MH  - Lipopolysaccharide Receptors/metabolism
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase/metabolism
MH  - Nuclear Proteins/metabolism
MH  - Prostaglandin-Endoperoxide Synthases/metabolism
MH  - Resuscitation
MH  - Shock, Hemorrhagic/metabolism/*physiopathology
MH  - Signal Transduction/physiology
MH  - Transcription Factors/metabolism
MH  - Up-Regulation
PMC - PMC7101685
EDAT- 2001/07/24 10:00
MHDA- 2001/11/03 10:01
PMCR- 2020/03/28
CRDT- 2001/07/24 10:00
PHST- 2001/04/19 00:00 [received]
PHST- 2001/04/21 00:00 [accepted]
PHST- 2001/07/24 10:00 [pubmed]
PHST- 2001/11/03 10:01 [medline]
PHST- 2001/07/24 10:00 [entrez]
PHST- 2020/03/28 00:00 [pmc-release]
AID - 242 [pii]
AID - 10.1007/s004230100242 [doi]
PST - ppublish
SO  - Langenbecks Arch Surg. 2001 Jul;386(4):302-8. doi: 10.1007/s004230100242.