Abstract | BACKGROUND/AIMS: METHODOLOGY: Pancreatic ischemia was achieved by occlusion of the 4 main pancreatic arteries for 40 min; this was followed by a 7-hour reperfusion period (group A, 10 rats). Outcome measures were compared with those of animals undergoing a sham operation (group B, 10 rats). RESULTS: Pancreatic damage in group A animals was demonstrated by increased serum alpha-amylase and by macroscopic and microscopic evidence. Total nitric oxide synthase activity in pancrease and lung was higher than in shams [median: 0.73 vs. 0.54 pmol/mg protein/min in the pancreas (P = 0.0082); 1.38 vs. 0.68 pmol/mg protein/min in the lung (P = 0.023)]; this was mainly due to activation of the inducible isoform of the enzyme. There was an associated 58.2% increase in plasma levels of nitric oxide metabolites [from mean 55.0 to 131.6 mumol/L (P < 0.001)]. Immunohistochemistry confirmed expression of inducible nitric oxide synthase and nitric oxide-mediated oxidative damage ( nitrotyrosine) in both pancreas and lung. CONCLUSIONS:
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Authors | G Viola, R A al-Mufti, M Sohail, R C Williamson, R T Mathie |
Journal | Hepato-gastroenterology
(Hepatogastroenterology)
2000 Sep-Oct
Vol. 47
Issue 35
Pg. 1250-5
ISSN: 0172-6390 [Print] Greece |
PMID | 11100325
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Nitric Oxide
- Nitric Oxide Synthase
- Nitric Oxide Synthase Type II
- Nos2 protein, rat
- alpha-Amylases
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Topics |
- Animals
- Disease Models, Animal
- Immunohistochemistry
- Lung
(enzymology)
- Male
- Nitric Oxide
(blood)
- Nitric Oxide Synthase
(metabolism)
- Nitric Oxide Synthase Type II
- Pancreas
(blood supply, enzymology)
- Rats
- Rats, Wistar
- Reperfusion Injury
(metabolism)
- alpha-Amylases
(blood)
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