PMID- 7537167
OWN - NLM
STAT- MEDLINE
DCOM- 19950601
LR  - 20220210
IS  - 1073-2322 (Print)
IS  - 1073-2322 (Linking)
VI  - 2
IP  - 2
DP  - 1994 Aug
TI  - Invited opinion: role of nitric oxide in hemorrhagic, traumatic, and anaphylactic 
      shock and thermal injury.
PG  - 145-55
AB  - The free radical nitric oxide (NO) is synthesized from the guanidino group of 
      L-arginine by a family of enzymes termed NO synthase (NOS). Hemorrhagic shock 
      leads to an inhibition of NO production by the calcium-dependent, endothelial NOS 
      (ecNOS), which may lead to maldistribution of blood flow leading to, e.g., 
      coronary, renal, and cerebral ischemia and may enhance the adhesion of neutrophil 
      granulocytes and platelets to the endothelial surface. Prolonged periods of 
      hemorrhagic shock are associated with the induction of a calcium-independent 
      isoform of NOS in a variety of organs and in the vascular smooth muscle. The 
      formation of large quantities of NO by inducible isoform of NOS (iNOS) 
      contributes to the delayed vascular decompensation and to the hyporeactivity of 
      the vasculature to vasoconstrictor agents. An impairment of NO formation by the 
      ecNOS has been demonstrated in various models of traumatic shock, whereas there 
      is good experimental evidence supporting the hypothesis that an enhanced 
      formation of NO contributes to the pathophysiology of experimental thermal injury 
      and anaphylactic shock. We speculate that a pharmacological modulation of NO 
      biosynthesis which either enhances NO concentration in the vicinity of 
      endothelium (i.e., NO donors) or inhibits NO overproduction following iNOS 
      expression (i.e., iNOS-selective NOS inhibitors) may become novel therapies to 
      improve the outcome of patients with circulatory shock of various etiologies.
FAU - Szabo, C
AU  - Szabo C
AD  - William Harvey Research Institute, St. Bartholomew's Hospital Medical Center, 
      London, United Kingdom.
FAU - Thiemermann, C
AU  - Thiemermann C
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Shock
JT  - Shock (Augusta, Ga.)
JID - 9421564
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 94ZLA3W45F (Arginine)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.4.- (Amino Acid Oxidoreductases)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
SB  - IM
MH  - Amino Acid Oxidoreductases/*metabolism
MH  - Anaphylaxis/*physiopathology
MH  - Animals
MH  - Arginine/analogs & derivatives/pharmacology
MH  - Burns/physiopathology
MH  - Endothelium, Vascular/physiology/*physiopathology
MH  - Humans
MH  - Liver Circulation/drug effects/physiology
MH  - Models, Biological
MH  - NG-Nitroarginine Methyl Ester
MH  - Nitric Oxide/antagonists & inhibitors/*physiology
MH  - Nitric Oxide Synthase
MH  - Shock/*physiopathology
MH  - Shock, Hemorrhagic/*physiopathology
MH  - Wounds and Injuries/*physiopathology
RF  - 125
EDAT- 1994/08/01 00:00
MHDA- 1994/08/01 00:01
CRDT- 1994/08/01 00:00
PHST- 1994/08/01 00:00 [pubmed]
PHST- 1994/08/01 00:01 [medline]
PHST- 1994/08/01 00:00 [entrez]
PST - ppublish
SO  - Shock. 1994 Aug;2(2):145-55.