PMID- 10357916
OWN - NLM
STAT- MEDLINE
DCOM- 19990708
LR  - 20131121
IS  - 0022-4804 (Print)
IS  - 0022-4804 (Linking)
VI  - 84
IP  - 2
DP  - 1999 Jun 15
TI  - Does upregulation of inducible nitric oxide synthase (iNOS) render the stomach 
      more susceptible to damage?
PG  - 174-9
AB  - Nitric oxide from constitutive nitric oxide synthase (NOS) augments gastric 
      mucosal blood flow and is important in mucosal defense. However, the function of 
      the inducible isoform of NOS (iNOS) in the gastric mucosa remains to be fully 
      elucidated. This study was done to examine the role of iNOS in gastric mucosal 
      blood flow and gastric injury following endotoxemia. Conscious rats were given 
      intraperitoneal saline or lipopolysaccharide (LPS, 5 or 20 mg/kg). Five hours 
      later, rats were anesthetized, a laparotomy made, gastric fluid aspirated, and 3 
      ml of 20% ethanol introduced into the forestomach. Rats were sacrificed 10 min 
      later for assessment of macroscopic injury (mm2) to the gastric mucosa. Other 
      rats did not receive 20% ethanol, but instead, gastric mucosal blood flow was 
      determined with laser Doppler, followed by sacrifice and removal of stomachs for 
      determination of gastric mucosal iNOS immunoreactivity (Western immunoblot). 
      Lipopolysaccharide dose dependently increased gastric injury, decreased gastric 
      mucosal blood flow, and increased gastric mucosal iNOS immunoreactivity compared 
      to rats receiving saline. In additional experiments and using a similar protocol, 
      intraperitoneal administration of aminoguanidine (45 mg/kg), an iNOS inhibitor, 
      reversed lipopolysaccharide-induced gastric injury and restored gastric mucosal 
      blood flow to baseline, whereas the nonselective NOS inhibitor, 
      NG-nitro-l-arginine methyl ester (5 mg/kg) did not. Taken together, these data 
      suggest that upregulation of iNOS is in part responsible for the detrimental 
      effects of LPS on the gastric mucosa, possibly from a reduction in gastric 
      mucosal blood flow.
CI  - Copyright 1999 Academic Press.
FAU - Castaneda, A A
AU  - Castaneda AA
AD  - Department of Surgery, University of Texas-Houston Medical School, Houston, 
      Texas, 77030, USA.
FAU - Denning, J W
AU  - Denning JW
FAU - Chang, L
AU  - Chang L
FAU - Mercer, D W
AU  - Mercer DW
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Surg Res
JT  - The Journal of surgical research
JID - 0376340
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Guanidines)
RN  - 0 (Lipopolysaccharides)
RN  - 3K9958V90M (Ethanol)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, rat)
RN  - SCQ4EZQ113 (pimagedine)
SB  - IM
MH  - Animals
MH  - Dose-Response Relationship, Drug
MH  - Drug Synergism
MH  - Endotoxemia/*enzymology/*pathology
MH  - Enzyme Inhibitors/pharmacology
MH  - Ethanol/pharmacology
MH  - Female
MH  - Gastric Mucosa/*blood supply
MH  - Guanidines/pharmacology
MH  - Lipopolysaccharides/antagonists & inhibitors/pharmacology
MH  - Nitric Oxide Synthase/*metabolism
MH  - Nitric Oxide Synthase Type II
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Regional Blood Flow/drug effects/physiology
MH  - Stomach/*enzymology/*pathology
EDAT- 1999/06/08 00:00
MHDA- 1999/06/08 00:01
CRDT- 1999/06/08 00:00
PHST- 1999/06/08 00:00 [pubmed]
PHST- 1999/06/08 00:01 [medline]
PHST- 1999/06/08 00:00 [entrez]
AID - S0022-4804(99)95637-8 [pii]
AID - 10.1006/jsre.1999.5637 [doi]
PST - ppublish
SO  - J Surg Res. 1999 Jun 15;84(2):174-9. doi: 10.1006/jsre.1999.5637.