Ischemic postconditioning attenuates renal ischemic/reperfusion injury in mongrel dogs.
OBJECTIVE
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Jiang
Botao
B
Department of Urology, Renmin Hospital of Wuhan University, Wuhan University, Wuhan, China.
Liu
Xiuheng
X
Chen
Hui
H
Liu
Dongshan
D
Kuang
Youling
Y
Xing
Bianzhi
B
Chen
Zhiyuan
Z
D000118:Acetylglucosaminidase / Q000652:urine; D000818:Animals; D017209:Apoptosis; D001806:Blood Urea Nitrogen; D003250:Constriction; D003404:Creatinine / Q000097:blood / Q000652:urine; D004285:Dogs; D020287:In Situ Nick-End Labeling; D057775:Ischemic Postconditioning / Q000379:methods*; D007668:Kidney / Q000098:blood supply* / Q000737:chemistry / Q000473:pathology; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000032:analysis; D008954:Models, Biological; D009195:Peroxidase / Q000032:analysis; D011897:Random Allocation; D015424:Reperfusion / Q000009:adverse effects / Q000379:methods; D015427:Reperfusion Injury / Q000097:blood / Q000209:etiology / Q000517:prevention & control* / Q000652:urine; D013482:Superoxide Dismutase / Q000032:analysis; D052096:Warm Ischemia / Q000009:adverse effects / Q000379:methods
D008315:Malondialdehyde; D003404:Creatinine; D009195:Peroxidase; D013482:Superoxide Dismutase; D000118:Acetylglucosaminidase