Linked Life Data

9843819

Source:http://linkedlifedata.com/resource/pubmed/id/9843819

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6 Pt 2
pubmed:dateCreated
1999-2-1
pubmed:abstractText
The anti-inflammatory role of nitric oxide (NO) was studied in a model of hepatic ischemia-reperfusion (I/R) in rats. Male Fischer rats were subjected to 30 min of no-flow ischemia of the left and median lobes of the liver, and animals were examined for a 4-h period of reperfusion. The animals were divided into the following groups: control-vehicle; I/R-vehicle; I/R-Nomega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg iv, 10 min before reperfusion); sham control-L-NAME, and I/R-S-nitroso-N-acetyl-penicillamine (SNAP, 25 micromol/kg iv, 10 min before reperfusion, followed by 20 micromol. kg-1. h-1 in 1.0 ml saline infused for 4 h). Results showed that mean arterial blood pressure was significantly increased in the sham control-L-NAME or I/R-L-NAME groups compared with either the I/R-vehicle or I/R-SNAP groups. However, cardiac index (CI) and stroke volume index (SVI) were markedly decreased, and systemic vascular resistance index (SVRI) was dramatically increased. Interestingly, the CI and SVI in rats treated with SNAP were markedly improved over that of the I/R group. Plasma nitrate and nitrite levels were significantly decreased in the I/R-L-NAME group; however, superoxide generation in the ischemic lobes and plasma alanine aminotransferase activity were higher compared with I/R-SNAP rats. The L-NAME-induced enhancement of hepatic injury in rats with I/R may be due in part to neutrophil infiltration, which was significantly increased compared with animals subjected to I/R or I/R-SNAP. The mechanism of L-NAME-enhanced neutrophil infiltration may be due to the fact that the ratios of P-selectin and intercellular adhesion molecule 1 (ICAM-1) mRNA to glyceraldehyde-3-phosphate dehydrogenase mRNA extracted from the ischemic lobes of I/R-L-NAME rats were significantly increased when compared with the I/R-SNAP group. These results suggest that 1) endogenous NO reduces the SVRI and permits an increased CI and SVI; 2) exogenous NO further improves CI and SVI; and 3) endogenous, but not exogenous, NO decreases P-selectin and ICAM-1 mRNA expression, thereby reducing polymorphonuclear neutrophil-dependent reperfusion tissue injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
275
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H2191-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9843819-Alanine Transaminase, pubmed-meshheading:9843819-Animals, pubmed-meshheading:9843819-Cell Adhesion Molecules, pubmed-meshheading:9843819-Hemodynamics, pubmed-meshheading:9843819-Intercellular Adhesion Molecule-1, pubmed-meshheading:9843819-Ischemia, pubmed-meshheading:9843819-Leukocyte Count, pubmed-meshheading:9843819-Liver Circulation, pubmed-meshheading:9843819-Male, pubmed-meshheading:9843819-Neutrophils, pubmed-meshheading:9843819-Nitrates, pubmed-meshheading:9843819-Nitric Oxide, pubmed-meshheading:9843819-Nitrites, pubmed-meshheading:9843819-P-Selectin, pubmed-meshheading:9843819-RNA, Messenger, pubmed-meshheading:9843819-Rats, pubmed-meshheading:9843819-Rats, Inbred F344, pubmed-meshheading:9843819-Reperfusion Injury, pubmed-meshheading:9843819-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
1998
pubmed:articleTitle
NO modulates P-selectin and ICAM-1 mRNA expression and hemodynamic alterations in hepatic I/R.
pubmed:affiliation
Department of Cell Biology, University of Medicine and Dentistry of New Jersey, School of Osteopathic Medicine, Stratford, New Jersey 08084, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't