2001
DOI: 10.1046/j.0007-1323.2001.01841.x
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Expression of inducible nitric oxide synthase contributes to the development of pancreatitis following pancreatic ischaemia and reperfusion

Abstract: Expression of iNOS during reperfusion following pancreatic ischaemia contributes significantly to the development of acute pancreatitis.

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Cited by 33 publications
(29 citation statements)
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“…Also, our observations confirmed that overproduction of NO arising from the iNOS was associated with the development of acute pancreatitis as shown by marked hyperamylasemia, increased pancreas water content, and histologically extensive acinar cell vacuolization. Our data confirm previous observations of enhanced iNOS expression and increased NO metabolites during acute pancreatitis (7,21,24,29,30). Because the amount of NO produced by cNOS is too small to be reflected in the changes of NO levels, the induction of iNOS, presumably in macrophages and vascular smooth cells, may be responsible for the large release of NO in acute pancreatitis (7).…”
Section: Discussionsupporting
confidence: 80%
“…Also, our observations confirmed that overproduction of NO arising from the iNOS was associated with the development of acute pancreatitis as shown by marked hyperamylasemia, increased pancreas water content, and histologically extensive acinar cell vacuolization. Our data confirm previous observations of enhanced iNOS expression and increased NO metabolites during acute pancreatitis (7,21,24,29,30). Because the amount of NO produced by cNOS is too small to be reflected in the changes of NO levels, the induction of iNOS, presumably in macrophages and vascular smooth cells, may be responsible for the large release of NO in acute pancreatitis (7).…”
Section: Discussionsupporting
confidence: 80%
“…NO overproduction by iNOS in the pancreas is implicated in the exacerbation of cell injury during AP (Lomis et al 1995;Viola et al 2000;Ayub et al 2001;Simsek et al 2001;Cuzzocrea et al 2002;Ozturk et al 2003;Um et al 2003;Chen et al 2004;Isik et al 2004;Sandstrom et al 2005). One possible mechanism of NO-mediated damage is potentiation of oxidative stress by NO.…”
Section: Mechanisms Of Ros and Rns Induced Damage In Pancreatic Acinamentioning
confidence: 99%
“…The role of NO produced by either constitutive or inducible NOS in experimental models of AP is controversial. Generally, NO generated by iNOS, which during AP is induced in infiltrating neutrophils and macrophages (Satoh et al 1998) and also in the other cells of pancreatic tissue (Al Mufti et al 1998;Rau et al 2001;Vaquero et al 2001;Qader et al 2003;Um et al 2003), has injurious effects (Lomis et al 1995;Ayub et al 2001;Simsek et al 2001;Cuzzocrea et al 2002;Ozturk et al 2003;Um et al 2003;Chen et al 2004;Isik et al 2004;Sandstrom et al 2005). The inducible form of cyclooxygenase, producing CO in a manner similar to NO production by iNOS, also exacerbates the severity of pancreatitis (Song et al 2002).…”
Section: No Links To Pancreatic Acinar Cell Homeostasis and Pathologymentioning
confidence: 99%
“…Our hypothesis that an overproduction of NO by ecNOS and/or iNOS plays a key role in the proposed pathophysiologic sequelae of acute pancreatitis is further supported by numerous studies demonstrating beneficial effects of nonselective NOS inhibitors in acute pancreatitis [149][150][151][152] as well as after pancreatic cold [153] and warm ischemia-reperfusion [154]. These beneficial effects include the prevention of progressive and severe hypotension [150], the reduction in multiorgan oxidative stress [149] and bacterial translocation [152], as well as the attenuation of diaphragmatic dysfunction [151] in acute experimental pancreatitis.…”
Section: Potential Candidates Mediating Vasoconstriction/vasodilationmentioning
confidence: 88%