Exogenous nitric oxide can control SIRS and downregulate NFκB1,2

Lozano, Francisco; Barros, Marcello Barbosa; García-Criado, Francisco Javier; Gómez‐Alonso, Alberto

doi:10.1016/j.jss.2004.08.029

Cited by 7 publications

(14 citation statements)

References 34 publications

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“…NFκB activity is inhibited by NO [45,56,57]. However, peroxynitrite (ONOO), which is formed from NO after reaction with radical oxygen intermittents, sustains NFκB activity [45].…”

Section: Resultsmentioning

confidence: 99%

Applied information retrieval and multidisciplinary research: new mechanistic hypotheses in Complex Regional Pain Syndrome

Hettne

Mos

Bruijn

et al. 2007

J Biomed Discov Collaboration

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Background: Collaborative efforts of physicians and basic scientists are often necessary in the investigation of complex disorders. Difficulties can arise, however, when large amounts of information need to reviewed. Advanced information retrieval can be beneficial in combining and reviewing data obtained from the various scientific fields. In this paper, a team of investigators with varying backgrounds has applied advanced information retrieval methods, in the form of text mining and entity relationship tools, to review the current literature, with the intention to generate new insights into the molecular mechanisms underlying a complex disorder. As an example of such a disorder the Complex Regional Pain Syndrome (CRPS) was chosen. CRPS is a painful and debilitating syndrome with a complex etiology that is still unraveled for a considerable part, resulting in suboptimal diagnosis and treatment.

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“…NFκB activity is inhibited by NO [45,56,57]. However, peroxynitrite (ONOO), which is formed from NO after reaction with radical oxygen intermittents, sustains NFκB activity [45].…”

Section: Resultsmentioning

confidence: 99%

Applied information retrieval and multidisciplinary research: new mechanistic hypotheses in Complex Regional Pain Syndrome

Hettne

Mos

Bruijn

et al. 2007

J Biomed Discov Collaboration

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“…It has been reported that NO produced via constitutive NOS (i.e., nNOS or eNOS) may be an important endogenous inhibitor of leukocyte-endothelial cell interactions, whereas high levels of NO associated with the induction of iNOS may be detrimental to targeted tissues/organs (Levy et al, 2005). Bacterial endotoxins and SIRS-relevant inflammatory cytokines, in contrast, have been shown to induce iNOS expression in various organs/ tissues, including intestine (Kleinert et al, 2003;Lozano et al, 2005). With respect to the latter, it has been shown that sustained up-regulation of NO production in the intestine leads to intestinal epithelial injury through the formation of peroxynitrite, a highly cytotoxic molecule capable of initiating lipid peroxidation and formation of nitrotyrosine (Potoka et al, 2002;Lush et al, 2003).…”

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confidence: 99%

Hindlimb Ischemia/Reperfusion-Induced Remote Injury to the Small Intestine: Role of Inducible Nitric-Oxide Synthase-Derived Nitric Oxide

Katada

Bihari²,

Badhwar³

et al. 2009

J Pharmacol Exp Ther

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Systemic inflammatory response syndrome, as a consequence of ischemia/reperfusion (I/R), negatively influences the function of the affected organs. The objective of this study was to assess the role of nitric oxide (NO) in remote intestinal inflammatory response elicited by hindlimb I/R. To this end, C57BL/6 (wild type; WT) and inducible nitric-oxide synthase (iNOS)-deficient mice were subjected to bilateral hindlimb ischemia (1 h) followed by 6 h of reperfusion. Some WT mice were injected with iNOS inhibitor N- [3-(aminomethyl)benzyl] acetamidine (1400W) (5 mg/kg s.c.) immediately before reperfusion, and proinflammatory response was assessed 6 h later. Hindlimb I/R resulted in dysfunction of the small intestine as assessed by the increase in permeability [blood-to-lumen clearance of Texas Red-dextran (molecular mass 3 kDa)] and an increase in the luminal levels of tumor necrosis factor (TNF)-␣ protein and nitrate/nitrite (NO 2 Ϫ /NO 3 Ϫ ). The above-mentioned changes were accompanied by up-regulation of the proinflammatory phenotype in the mucosa of small intestine with respect to 1) an increase in TNF-␣ and iNOS protein expression, 2) leukocyte accumulation, 3) formation of edema, 4) an increase in leukocyte rolling/adhesion in the submucosal microvasculature, and 5) activation of transcription factor nuclear factor-B and upregulation of adhesion molecule expression. Interestingly, the most profound changes with respect to intestinal dysfunction were found in jejunum and ileum, whereas duodenum was affected the least. Interfering with iNOS activity (1400W and iNOS-deficient mice) significantly attenuated hindlimb I/R-induced inflammatory response and dysfunction of the small intestine with respect to the above-mentioned markers of inflammation. The obtained results indicate that hindlimb I/R induces remote inflammatory response in the small intestine through an iNOS-derived NO-dependent mechanism.

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“…Las prótesis y biomateriales utilizadas en cualquier tipo de cirugía reconstructiva provocan una respuesta inflamatoria crónica (311,298,5) . La regulación de la respuesta inflamatoria podría ser una estrategia para disminuir ó limitar el daño tisular en los pacientes quirúrgicos que precisan la colocación de una prótesis (9,276,186,108,39,175,220,121,186,160,248,120) , siendo especialmente relevante el control de la respuesta inflamatoria en la cirugía aórtica.…”

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“…Así mismo, las reparaciones del AAA representan un desafío para el cirujano vascular por las complicaciones derivadas de los clampajes y desclampajes de la aorta, con fases de isquemia seguidas de periodos de reperfusión que van a originar profundas agresiones fisiológicas en casi todos los sistemas orgánicos, desencadenando una respuesta inflamatoria sistémica (8) . Se ha investigado mucho sobre el papel que podría jugar el óxido nítrico (NO) en el proceso inflamatorio, y en concreto en los procesos secundarios a isquemia-reperfusión, otorgándole últimamente un efecto protector (186) . El óxido nítrico es un mediador importante de la respuesta inflamatoria, y un aumento de sus niveles puede proteger de la lesión renal causada por el clampaje aórtico durante la reparación del aneurisma aórtico (258,188,98,248,173,39,220,228,186,187,121,175,108,160) .…”

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“…Se ha investigado mucho sobre el papel que podría jugar el óxido nítrico (NO) en el proceso inflamatorio, y en concreto en los procesos secundarios a isquemia-reperfusión, otorgándole últimamente un efecto protector (186) . El óxido nítrico es un mediador importante de la respuesta inflamatoria, y un aumento de sus niveles puede proteger de la lesión renal causada por el clampaje aórtico durante la reparación del aneurisma aórtico (258,188,98,248,173,39,220,228,186,187,121,175,108,160) . En modelos de isquemia-reperfusión renal (74) se ha comprobado como el NO juega un papel muy importante en la regulación del flujo renal, así como en la excreción de sodio y agua en condiciones fisiológicas y durante el fallo renal agudo secundario a isquemia-reperfusión.…”

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Respuesta inflamatoria y cirugía protésica. Su control con donadores de óxido nítrico

Rosás¹

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Exogenous nitric oxide can control SIRS and downregulate NFκB1,2

Cited by 7 publications

References 34 publications

Applied information retrieval and multidisciplinary research: new mechanistic hypotheses in Complex Regional Pain Syndrome

Applied information retrieval and multidisciplinary research: new mechanistic hypotheses in Complex Regional Pain Syndrome

Hindlimb Ischemia/Reperfusion-Induced Remote Injury to the Small Intestine: Role of Inducible Nitric-Oxide Synthase-Derived Nitric Oxide

Respuesta inflamatoria y cirugía protésica. Su control con donadores de óxido nítrico

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