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Departments of 1 Cell Biology and 2 Molecular Biology, University of Medicine and Dentistry of New Jersey, School of Osteopathic Medicine, Stratford, New Jersey 08084
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-N
-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 µmol/kg iv, 10 min before reperfusion, followed by 20 µmol · kg
1 · h1
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.
nitric oxide synthase; systemic vascular resistance index; reverse transcription-polymerase chain reaction; ischemia-reperfusion
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