Biphasic role for nitric oxide in experimental renal warm ischaemia–reperfusion injury

Weight, S. C.; Furness, Peter; Nicholson, Michael L.

doi:10.1046/j.1365-2168.1999.01162.x

Cited by 23 publications

(20 citation statements)

References 41 publications

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“…2,39,[41][42][43] Reactive oxygen and nitrogen species are believed to play a central role in I/R injury in addition to several other factors, such as neutrophils, platelets, the coagulation system and the xanthine-oxidoreductase enzyme system. Our previous report demonstrated that renal I/R worsened the renal dysfunction, oxidative stress and histopathologic features in rats.…”

Section: Discussionmentioning

confidence: 99%

Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion injury

Korkmaz

Kolankaya

2013

Can J Surg

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Background: Nitric oxide (NO) seems to play an important role during renal ischemia/reperfusion (I/R) injury. We investigated whether rutin inhibits inducible nitric oxide synthase (iNOS) and reduces 3-nitrotyrosine (3-NT) formation in the kidneys of rats during I/R. Methods:Wistar albino rats were nephrectomized unilaterally and, 2 weeks later, subjected to 45 minutes of left renal pedicle occlusion followed by 3 hours of reperfusion. We intraperitoneally administered L-N6-(1-iminoethyl)lysine (L-NIL; 3 mg/kg) for 30 minutes or rutin (1 g/kg) for 60 minutes before I/R. After reperfusion, kidney samples were taken for immunohistochemical analysis of iNOS and 3-NT. We measured plasma nitrite/nitrate and cyclic guanosine monophosphate (cGMP) to evaluate NO levels.Results: Ischemia/reperfusion caused plasma cGMP to increase significantly. Similarly, plasma nitrite/nitrate was elevated in the I/R group compared with the control group. Histochemical staining was positive for iNOS and 3-NT in the I/R group. Pretreatment with L-NIL or rutin significantly mitigated the elevation of plasma cGMP and nitrite/nitrate. These changes in biochemical parameters were also associated with changes in immunohistochemical appearance. Pretreatment with L-NIL or rutin significantly decreased the incidence and severity of iNOS and 3-NT formation in the kidney tissues. Conclusion:Our findings suggest that high activity of iNOS causes renal I/R injury, and that rutin exerts protective effects, probably by inhibiting iNOS.Contexte : L'oxyde nitrique (NO) semble jouer un rôle important durant la lésion d'ischémie/reperfusion (I/R) rénale. Nous avons vérifié si la rutine inhibe l'oxyde nitrique synthase inductible (iNOS) et réduit la formation de 3-nitrotyrosine (3-NT) dans les reins de rats durant l'I/R. Méthodes :Des rats albinos Wistar ont subi une néphrectomie unilatérale avant d'être soumis 2 semaines plus tard à une occlusion du pédicule rénal gauche d'une durée de 45 minutes, suivie de 3 heures de reperfusion. Nous avons administré de la L-N6-(1-iminoéthyl)lysine (L-NIL; 3 mg/kg) par voie intrapéritonéale pendant 30 minutes ou de la rutine (1 g/kg) pendant 60 minutes avant l'I/R. Après la reperfusion, des échantillons de tissu rénal ont été prélevés pour analyse immunohistochi mique de l'iNOS et de la 3-NT. Nous avons mesuré les taux plasmatiques de nitrite/nitrate et de guanosine monophosphate cyclique (cGMP) pour évaluer les taux de NO.

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Section: Discussionmentioning

confidence: 99%

Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion injury

Korkmaz

Kolankaya

2013

Can J Surg

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“…However, it has been demonstrated that NO plays a biphasic role in pathophysiology of renal injury mediated by I/R [30]. In early phases, the increased oxidative and nitrosative damage was exacerbated by NO donors but ameliorated by NOS inhibition [5,30].…”

Section: Discussionmentioning

confidence: 99%

Effects of trapidil on renal ischemia-reperfusion injury

Avlan

Tamer

Ayaz

et al. 2006

Journal of Pediatric Surgery

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“…They further alleged that NOS played a cytotoxic role in the early stages while it had a cytoprotective role in the late stages. Other researchers have also examined the biphasic effect of NO [9,10] .…”

Section: Discussionmentioning

confidence: 99%

Role of Glyceryl Trinitrate, a Nitric Oxide Donor, in the Renal Ischemia-Reperfusion Injury of Rats

Küçük¹,

Kaptanoğlu²,

Ozalp³

et al. 2006

Eur Surg Res

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Background/Aims: Ischemia-reperfusion injury is a serious clinical situation which can cause serious morbidity and mortality. An experimental renal ischemia-reperfusion injury model was designed to evaluate the role of glyceryl trinitrate (GTN) on renal function and histology. Methods: 50 Wistar albino rats were used in our study. Five groups were formed: (1) sham-control group; (2) acute renal ischemia (ARI) group with placebo (0.9% NaCl) infusion; (3) GTN infusion with a 75 µg/kg/min dose prior to ARI was administered; (4) GTN infusion with a 150 µg/kg/min dose prior to ARI was given, and finally (5) 150 µg/kg/min GTN infusion after the ARI period was applied. Serum BUN and creatinine levels were measured for evaluation of renal function. T_max-sec, glomerular filtration rate (GFR), and T_max-min results following a ^99mTc-DTPA diuretic renal scintigraphy were used. Histological examination was performed on nephrectomy specimens. Results: Groups 2 and 5 showed higher BUN, creatinine, and lower GFR values than the other groups (p = 0.0001). There was no difference in BUN, creatinine, and GFR levels between groups 2 and 5 (p = 0.971, p = 0.739, p = 0.393). Also the T_max-sec values were higher in groups 2 and 5 compared with the other groups (p = 0.0001). The presence of tubular necrosis was different between groups and was higher in groups 2 and 5 (p = 0.002). Conclusion: The application of GTN, a nitric oxide donor, has caused significant improvement in renal function when applied prior to an experimentally designed renal ischemia-reperfusion model. But administration of GTN had no effect after occurrence of ischemia.

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Biphasic role for nitric oxide in experimental renal warm ischaemia–reperfusion injury

Abstract: Inhibition of the postischaemic increase in the level of nitric oxide was associated with an early decrease in, but eventual exacerbation of, oxidative damage. This suggests the prolonged increase in renal nitric oxide concentration was cytoprotective overall.

Cited by 23 publications

References 41 publications

Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion injury

Inhibiting inducible nitric oxide synthase with rutin reduces renal ischemia/reperfusion injury

Effects of trapidil on renal ischemia-reperfusion injury

Role of Glyceryl Trinitrate, a Nitric Oxide Donor, in the Renal Ischemia-Reperfusion Injury of Rats

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