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Updated: Oct 8, 2026

Renal Ischaemia Reperfusion Injury: A Mouse Model of Injury and Regeneration
Published on: June 7, 2014
Role of the L-arginine/nitric oxide pathway in renal ischaemia-reperfusion in rats
E L Rhoden1, L Pereira-Lima, C R Rhoden
1Medical Clinic of the Clinical Hospital of Porto Alegre, RS, Brazil. ernanirhod@cpovo.net
Objective:
To study the role of the L-arginine/nitric oxide (NO) pathway during renal ischaemia-reperfusion in rats.
Design:
Randomised experimental study.
Setting:
Teaching hospital, Brazil.
Animals:
97 male Wistar rats randomly assigned to 4 groups for the assessment of renal dysfunction and to 6 groups for the assessment of the oxidative stress induced on renal cell membranes by ischaemia-reperfusion.
Interventions:
The animals underwent sham-operation or renal ischaemia-reperfusion (n = 9 each) with or without pretreatment with L-arginine (a NO donor) or L-NAME (N(omega)-nitro-L-arginine methyl ester--an inhibitor of NO production) (n = 10 each).
Main Outcome Measures:
Serum creatinine concentrations and oxidative stress by chemiluminescence initiated by the tert-butyl hydroperoxide technique.
Results:
Renal ischaemia-reperfusion significantly worsened renal dysfunction and increased oxidative stress in the ischaemia-reperfusion group after 24 and 96 hours of reperfusion compared with the control group (p < 0.05). Pretreatment with L-NAME slightly but not significantly increased serum creatinine concentrations after 24 and 96 hours of reperfusion together with activity of reactive oxygen species during renal ischaemia-reperfusion. L-arginine also significantly protected renal function and reduced the increment in the amount of chemiluminescence induced by giving L-NAME during 24 and 96 hours of reperfusion (p < 0.05).
Conclusion:
The L-arginine/NO pathway seems to have a slightly protective effect on the kidney after renal ischaemia-reperfusion injury in rats. These results need to be confirmed by studies in human beings.
