Intestinal nitric oxide synthase activity changes during experimental colon obstruction

Palásthy, Zsolt; Kaszaki, József; Lázár, György; Nagy, S.; Boros, Mihály

doi:10.1080/00365520600548966

Cited by 9 publications

(14 citation statements)

References 25 publications

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“…In this canine model, experimental blockade of the intestinal passage increased the large bowel motility, and triggered a hyperdynamic circulatory reaction 5 h after obstruction, accompanied by significant NO production, XO activation and leucocyte accumulation in the proximal colon. This hyperdynamic cardiovascular response may be regarded as a compensatory reaction through which the organism tries to accommodate to the evolving septic metabolic changes 28,29 …”

Section: Discussionmentioning

confidence: 99%

“…32 have demonstrated that low doses of endotoxin cause marked changes in myoelectric activity in the small intestine, with repetitive bursts of spike potentials and a simultaneous increase in the transit of the intestinal contents. Indeed, the obstruction‐induced motility alterations are time‐dependent, characteristically changing in parallel with the development of inflammation 28,33,34 …”

Section: Discussionmentioning

confidence: 99%

“…This hyperdynamic cardiovascular response may be regarded as a compensatory reaction through which the organism tries to accommodate to the evolving septic metabolic changes. 28,29 Conflicting data have been reported on inflammation-induced motility alterations. It was recently suggested that, in proinflammatory conditions, the activation of resident macrophages in the tunica muscularis and the upregulation of cytokines may affect the smooth muscle contractility.…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, the obstruction-induced motility alterations are time-dependent, characteristically changing in parallel with the development of inflammation. 28,33,34 The MPO activity is a quantitative marker of the leucocytes accumulated in various tissues. 27 A decreased MPO activity was found in the obstructed colon segment following KynA treatment, and this could be related to the partial elimination of XORdependent oxygen radical production.…”

Section: Discussionmentioning

confidence: 99%

“…The CO was determined by thermodilution, using a SPEL Advanced Cardiosys 1.4 computer (Experimetria Ltd). The total peripheral vascular resistance (TPR) 28 was calculated via the standard formula (MAP − CVP/CO).…”

Section: Methodsmentioning

confidence: 99%

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Kynurenic acid inhibits intestinal hypermotility and xanthine oxidase activity during experimental colon obstruction in dogs

Kaszaki

Palásthy

Erczes

et al. 2007

Neurogastroenterology Motil

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Kynurenic acid (KynA), an endogenous antagonist of N-methyl-d-aspartate (NMDA) glutamate receptors, protects the central nervous system in excitotoxic neurological diseases. We hypothesized that the inhibition of enteric glutamate receptors by KynA may influence dysmotility in the gastrointestinal tract. Group 1 of healthy dogs served as the sham-operated control, in group 2, the animals were treated with KynA, while in groups 3 and 4 mechanical colon obstruction was maintained for 7 h. Group 4 was treated with KynA at the onset of ileus. Hemodynamics and motility changes were monitored, and the activities of xanthine oxidoreductase (XOR) and myeloperoxidase (MPO) were determined from tissue samples. Colon obstruction induced a hyperdynamic circulatory reaction, significantly elevated the motility index and increased the mucosal leucocyte accumulation and the XOR activity. The KynA treatment augmented the tone of the colon, permanently decreased the motility index of the giant colonic contractions and reduced the increases in XOR and MPO activities. These effects were concomitant with the in vitro inhibition of XOR activity. In conclusion, KynA antagonizes the obstruction-induced motility responses and XOR activation in the colon. Inhibition of enteric NMDA receptors may provide an option to influence intestinal hypermotility and inflammatory changes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

Kynurenic acid inhibits intestinal hypermotility and xanthine oxidase activity during experimental colon obstruction in dogs

Kaszaki

Palásthy

Erczes

et al. 2007

Neurogastroenterology Motil

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Kynurenines and intestinal neurotransmission: the role of N-methyl-d-aspartate receptors

et al. 2011

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Gastrointestinal neuroprotection involves the net effect of many mechanisms which protect the enteral nervous system and its cells from death, dysfunction or degeneration. Neuroprotection is also a therapeutic strategy, aimed at slowing or halting the progression of primary neuronal loss following acute or chronic diseases. The neuroprotective properties of a compound clearly have implications for an understanding of the mechanism of dysfunctions and for therapeutic approaches in a number of gastrointestinal diseases.This paper focused on the roles of glutamate and N-methyl-D-aspartate (NMDA) receptors in the intrinsic neuronal control of gastrointestinal motility; the consequences of inflammation on gastrointestinal motility changes; and the involvement of tryptophan metabolites (especially kynurenic acid) in the regulatory function of the enteral nervous system and the modulation of the inflammatory response. Common features in the mechanisms of action, illustrative evidence from animal models, and experimental neuroprotective therapies making use of the currently available possibilities are also discussed.Overall, the evidence suggests that gastrointestinal neuroprotection against inflammation and glutamate-induced neurotoxicity may be mediated synergistically through the blockade of NMDA receptors and the inhibition of neuronal nitric oxide synthase activity and xanthine oxidoreductase-dependent superoxide production. These components are likewise significant factors in the pathomechanism of gastrointestinal inflammatory diseases and inflammation-linked motility alterations. Inhibition of the enteric NMDA receptors by kynurenic acid or its analogues may provide a novel option via which to influence intestinal hypermotility and inflammatory processes simultaneously.

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Nitric oxide bioavailability affects cardiovascular regulation dependent on cardiac nerve status

Kingma

Simard

Rouleau

2015

Autonomic Neuroscience

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Intestinal nitric oxide synthase activity changes during experimental colon obstruction

Cited by 9 publications

References 25 publications

Kynurenic acid inhibits intestinal hypermotility and xanthine oxidase activity during experimental colon obstruction in dogs

Kynurenic acid inhibits intestinal hypermotility and xanthine oxidase activity during experimental colon obstruction in dogs

Kynurenines and intestinal neurotransmission: the role of N-methyl-d-aspartate receptors

Nitric oxide bioavailability affects cardiovascular regulation dependent on cardiac nerve status

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