Renal ischaemic preconditioning and reperfusion injury: The role of nitric oxide

Original article


M Jefayri, P Grace, R Mathie

JMJ Vol. 2. No.1 [March] 2002: 41-47


Objective: To demonstrate the effect on nitric oxide (NO) release and renal NO synthase, endothelial (eNOS) and inducible (iNOS) activity of renal ischaemia – reperfusion (I / R) in vivo, in an animal model. The possible involvement of NO in ischaemic preconditioning (IP) of the kidney was also examined
Methods: in a right nephrectomised rat model, 42animals were randomized in four group: controls; IP – only (four min of ischaemia followed by 11min of reperfusion, total of four cycles); renal warm ischaemia (45min) and six hours reperfusion; ischaemia (45min) preceded by IP pre- treatment. Serum NO metabolites were assay after two hours and six hours after ischaemia or the control equivalent. NOS expression in kidney and morphological assessment of damage were identified by immunohistochemistry and haematoxylin and eosin staining respectively. Kidney function was assessed by serum creatinine, urea and electrolytes. Results: compared to pre-ischaemia, the concentration of serum NO metabolites at six hours were raised in IP- only animals (0.016) and in the (IP + I / R) group (p=0.002). There was increased eNOS expression in the IP-only group (p=0.009) and in the (IP + I / R) group compared to controls (p=0.050) iNOS Expression was increased in IP-only animals compared with the control group (p=0.050). Histological assessment showed less evidence of cellular damage in (IP +I / R) animals compared I/R alone (p=0.020). Serum creatinine showed no significant difference in the IP-only group compared to control. NO differences were observed at two hours reperfusion. Conclusion: ischaemic preconditioning elicits a protective effect on renal structure and function, which may be produced by increased NO release arising from increased NOS expression by six hours after reperfusion.

Keywords: Nitric oxide (NO), Endothelial (eNOS), inducible (iNOS)