P-344 The evaluation of the induction of inducible nitric oxide synthase in gastric mucosa and gastric mucosal blood flow in portal hypertensive gastropathy

1995 ◽  
Vol 3 ◽  
pp. S122
Author(s):  
A IRISAWA
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Gastric Mucosa ◽  
Inducible Nitric Oxide Synthase ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Portal Hypertensive Gastropathy ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Decreased endothelial nitric oxide synthase in gastric mucosa of rats with chronic renal failure

1998 ◽  
Vol 274 (6) ◽  
pp. F1102-F1108 ◽  
Author(s):  
M. Tomikawa ◽  
M. Ohta ◽  
N. D. Vaziri ◽  
J. D. Kaunitz ◽  
R. Itani ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Chronic Renal Failure ◽  
Nitric Oxide Synthase ◽  
Gastric Mucosa ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Enos Mrna ◽  
Oxide Synthase

According to recent reports, chronic renal failure (CRF) increases the susceptibility of gastric mucosa to injury. Since nitric oxide plays a major role in gastric mucosal defense and injury, we investigated, in rats with CRF produced by five-sixths nephrectomy and in control rats, the expression of nitric oxide synthase (NOS) in the stomach and measured mucosal and submucosal gastric blood flow. In CRF rats, gastric mucosal blood flow was significantly reduced compared with control rats, whereas submucosal and serosal blood flow was significantly increased. CRF significantly decreased endothelial NOS (eNOS) mRNA abundance by 53% ( P < 0.01) and reduced expression of eNOS protein by 42% ( P < 0.01) compared with the controls. Enzyme activity of eNOS was significantly reduced in gastric mucosa of CRF rats ( P < 0.05). These data are consistent with reduced gastric mucosal blood flow in CRF rats and can explain altered susceptibility of gastric mucosa to injury in CRF rats.

NEUTROPHIL ACCUMULATION AND DAMAGE TO THE GASTRIC MUCOSA IN RESUSCITATED HEMORRHAGIC SHOCK IS INDEPENDENT OF INDUCIBLE NITRIC OXIDE SYNTHASE

Shock ◽  
1999 ◽  
Vol 11 (5) ◽  
pp. 319-324 ◽  
Author(s):  
Katsuhiko Tsukada ◽  
Laurel A. Omert ◽  
John Menezes ◽  
Brian G. Harbrecht ◽  
Masayuki Miyagishima ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Gastric Mucosa ◽  
Hemorrhagic Shock ◽  
Inducible Nitric Oxide Synthase ◽  
Neutrophil Accumulation ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Reperfusion injury is reduced in skeletal muscle by inhibition of inducible nitric oxide synthase

2003 ◽  
Vol 94 (4) ◽  
pp. 1473-1478 ◽  
Author(s):  
Li Zhang ◽  
Colin G. Looney ◽  
Wen-Ning Qi ◽  
Long-En Chen ◽  
Anthony V. Seaber ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Reperfusion Injury ◽  
Inducible Nitric Oxide Synthase ◽  
Ischemia Reperfusion ◽  
Inos Inhibitor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

This study evaluated the effects of the selective inducible nitric oxide synthase (iNOS) inhibitor N-[3-(aminomethyl)benzyl]acetamidine (1400W) on the microcirculation in reperfused skeletal muscle. The cremaster muscles from 32 rats underwent 5 h of ischemia followed by 90 min of reperfusion. Rats received either 3 mg/kg 1400W or PBS subcutaneously before reperfusion. We found that blood flow in reperfused muscles was <45% of baseline in controls but sharply recovered to near baseline levels in 1400W-treated animals. There was a significant ( P < 0.01 to P< 0.001) difference between the two groups at each time point throughout the 90 min of reperfusion. Vessel diameters remained <80% of baseline in controls during reperfusion, but recovered to the baseline level in the 1400W group by 20 min, and reached a maximum of 121 ± 14% (mean ± SD) of baseline in 10- to 20-μm arterioles, 121 ± 6% in 21- to 40-μm arterioles, and 115 ± 8% in 41- to 70-μm arteries ( P < 0.01 to P < 0.001). The muscle weight ratio between ischemia-reperfused (left) and non-ischemia-reperfused (right) cremaster muscles was 193 ± 42% of normal in controls and 124 ± 12% in the 1400W group ( P < 0.001). Histology showed that neutrophil extravasation and edema were markedly reduced in 1400W-treated muscles compared with controls. We conclude that ischemia-reperfusion leads to increased generation of NO from iNOS in skeletal muscle and that the selective iNOS inhibitor 1400W reduces the negative effects of ischemia-reperfusion on vessel diameter and muscle blood flow. Thus 1400W may have therapeutic potential in treatment of ischemia-reperfusion injury.

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