Abstract

To investigate the effect of Postcond on renal ischemia-reperfusion (I/R) injury in a canine model. I/R injury is the most common cause of renal dysfunction. Ischemic postconditioning (Postcond) is a phenomenon by which intermittent interruptions of blood flow in the early phase of reperfusion can protect organs from I/R injury. Forty adult male mongrel dogs were randomly divided into five groups of eight dogs each. Animals underwent 60 minutes of renal pedicle occlusion followed by reperfusion for 72 hours. Postcond was performed by 15-second, 30-second, or 1-minute I/R for six or three cycles. Blood and urine were collected at different reperfusion time points (24, 48, and 72 hours), and blood urea nitrogen (BUN), creatinine (Cr) levels, urine N-acetyl-β-D-glucosaminidase (NAG), and Cr levels were assayed. Kidney samples were harvested after I/R, and renal superoxide dismutase (SOD), malondialdehyde (MDA), and myeloperoxidase (MPO) concentrations were measured, respectively. Apoptosis was evaluated by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling (TUNEL) assay in the tissue samples. Compared with the sham group, I/R resulted in renal dysfunction, decreased SOD levels, increased MDA and MPO levels, and increased apoptosis indexes. However, Postcond attenuated the aforementioned effects, the protection of which in the Postcond of 15-second reperfusion/ischemia for six cycles was the most notable. Postcond exerts protective effects on renal (I/R) injury. It may be a promising strategy against I/R injury in clinical practice. Its mechanisms may involve reduction of lipid peroxidation and cellular apoptosis.

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