Inhibition of Inducible Nitric Oxide Synthase Reduces Bacterial Translocation in a Rat Model of Acute Pancreatitis

Şimşek, İsmail; Refik, Mehmet; Yaşar, Mehmet; Özyurt, Mustafa; Sağlamkaya, Uğur; Deveci, Salih; Cömert, Bilgin; Başustaoğlu, Ahmet; Kocabalkan, Fikri

doi:10.1097/00006676-200110000-00011

Cited by 25 publications

(20 citation statements)

References 27 publications

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“…To investigate the pathophysiologic role of NO, a direct modulation of the NO pathway by application of either endogenous NOS inhibitors or NO donors was chosen in animal models of acute pancreatitis (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25). However, controversial results were obtained as to whether the effects of enhanced NO generation are positive, negative, or negligible with respect to the development of local and systemic complications in the course of the disease.…”

Section: Discussionmentioning

confidence: 99%

“…L-NAME, competitive NOS inhibitor, has been shown to prevent lung injury in acute pancreatitis model (24). Further, animal studies also have documented that the administration of a selective iNOS inhibitor reduces bacterial translocation in acute pancreatitis and appears to have ameliorated the course of disease (25). Therefore, inhibition of NOS had favorable effects on pancreatitis which is complicated by the condition in which iNOS is expressed to produce excessive amounts of NO.…”

Section: Discussionmentioning

confidence: 99%

“…These findings suggest that the overproduction of NO by iNOS plays an important role in the hemodynamic disturbances and cellular damage of several inflammatory states. Several investigators have examined the role of NO in various animal models of acute pancreatitis (14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24)(25). However, conflicting results have been reported.…”

Section: Introductionmentioning

confidence: 99%

“…There are several lines of evidence showing that NO seems to have a protective effect on local pancreatic cellular damage, mainly by inhibition of neutrophil accumulation and improvement of microcircula-tion (14)(15)(16)(17)(18)(19). In contrast, several reports suggest that inhibition of NOS or iNOS has a beneficial effect in experimental pancreatitis (20)(21)(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

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The Role of Nitric Oxide in Experimental Cerulein Induced Pancreatitis

Kwon

Kim

et al. 2003

J Korean Med Sci

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An enhanced formation of nitric oxide (NO), due to the induction of inducible nitric oxide synthase (iNOS), has been implicated in the pathogenesis of shock and inflammation, but its role in acute pancreatitis still remains controversial. To clarify the role of NO in acute pancreatitis, the present experiment investigated the expression of iNOS and the effect of NOS inhibition on cerulein-induced pancreatitis in rats. Group I received intraperitoneal (ip) injection of normal saline. Group II received two ip injections of cerulein (20 g/kg). Group III received injections of N G -nitro-L-arginine methyl ester (L-NAME) (30 mg/kg) with cerulein. Group IV received Larginine (250 mg/kg) with cerulein and L-NAME. The expression of iNOS in the pancreas was examined by western blot analysis. The plasma concentration of NO metabolites was measured. The severity of pancreatitis was assessed by measuring serum amylase, pancreas water content and histopathological examination. Compared with controls, the cerulein group displayed significantly increased expression of iNOS and raised plasma NO metabolites. Treatment with L-NAME significantly decreased hyperamylasemia, plasma NO level, and the extent of pancreatic injury. Treatment with L-arginine reversed the effects of L-NAME. These findings suggest that an enhanced formation of NO by iNOS plays an important role in the development of acute pancreatitis, and inhibition of NO production has the beneficial effects in reducing pancreas injury.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Role of Nitric Oxide in Experimental Cerulein Induced Pancreatitis

Kwon

Kim

et al. 2003

J Korean Med Sci

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“…In severe AP, inducible nitric oxide synthase (iNOS) overproduces NO. Excessive NO production cause pathological vasodilatation with capillary permeability increase and third space fluid loss 16 and tissue injury by NO derived free-radicals overproduction. AL MUFTI et al (1998) demonstrated an increase in iNOS activity associated to systemic NO increase and arterial hypotension in AP experimental models.…”

Section: Discussionmentioning

confidence: 99%

Methylene blue improves hemodynamic shock but increases lipoperoxidation in severe acute pancreatitis pig model

et al. 2008

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PURPOSE: Study hemodynamic pattern and lipoperoxidation during methylene blue (MB) treatment on taurocholate - enterokinase induced acute pancreatitis (AP). METHODS: Thirty pigs were equally divided in control group; MB group; AP group; MB previous AP group; and MB after 90 min of induced AP group. MB was given iv in a bolus dose (2mg.kg-1) followed by maintenance dose (2 mg.kg-1.h-1). Hemodynamic parameters were recorded continuously during 180 min by Swan-Ganz catheter. Blood samples were taken every 60 min to determine arterial and venous nitrate, malondialdehyde (MDA) and amylase. Pancreatic tissue was removed for histopathologic study. RESULTS: In AP group MBP and CO decreased over time 33% (p<0.05) and 52% (p<0.05), respectively. In MB previous induced-AP group, there was 70 minutes delay (p<0.05) to decrease MBP and CO. In MB group arterial and venous nitrite decreased (p<0.05) over time. MB infusion increased (p>0.05) serum MDA when associated to AP. After induced AP, MB did not reverse MBP and CO decrease. There was no difference in serum amylase and necro-hemorrhagic findings with MB treatment. CONCLUSIONS: In this taurocholate-induced AP model MB treatment delayed hemodynamic shock and decreases serum nitrate levels but increases serum MDA levels. No volemic replacement was done and it may have been a mitigated factor to a poor tissue perfusion and impairment microcirculation. Further investigations are needed to elucidate MB treatment role during AP treatment.

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Hyperbaric oxygen-induced changes in bacterial translocation and acinar ultrastructure in rat acute necrotizing pancreatitis

et al. 2005

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Inhibition of Inducible Nitric Oxide Synthase Reduces Bacterial Translocation in a Rat Model of Acute Pancreatitis

Abstract: Treatment with SMT appears to have ameliorated the course of acute pancreatitis; however, mortality was not affected.

Cited by 25 publications

References 27 publications

The Role of Nitric Oxide in Experimental Cerulein Induced Pancreatitis

The Role of Nitric Oxide in Experimental Cerulein Induced Pancreatitis

Methylene blue improves hemodynamic shock but increases lipoperoxidation in severe acute pancreatitis pig model

Hyperbaric oxygen-induced changes in bacterial translocation and acinar ultrastructure in rat acute necrotizing pancreatitis

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