| Ischemic postconditioning(IPO) is defined as rapid intermittent interruptions of blood flow in the early phase of reperfusion and mechanically alters the hydrodynamics of reperfusion. With ischemic preconditioning(IPC), IPO have protective effects against myocardial injury. However, IPO which attenuate renal ischemic/reperfusion(I/R) in a canine model has not been reported previously. The results of canine kidney with and without IPO after 1 h of warm ischemic were reported and the effects of IPO on prevention of chronic kidney fibrosis were investigated in this studies.PartⅠIschemic postconditioning improves renal dysfunction and the morphological features after renal ischemic/reperfusion in a canine modelObjective:To investigate the effect of IPO on the renal I/R injury in a canine model.Methods:Thirty adult male mongrel dogs were randomly divided into five groups with 6 animals in each group:group 1, sham-operated group; group 2, I/R group; group 3,6x15 seconds IPO group, kidneys were subjected to six cycles of 15 seconds of reperfusion followed by 15 seconds of ischemia immediately after 60 minutes of ischemia; group 4,6×30 seconds IPO group, kidneys were subjected to six cycles of 30 seconds of reperfusion followed by 30 seconds of ischemia immediately after 60 minutes of ischemia; group 5,3×1 minute IPO group, kidneys were subjected to three cycles of 1 minute of reperfusion followed by 1 minute of ischemia immediately after 60 minutes of ischemia. Samples of blood and urine were collected at different reperfusion time point (24h,48h and 72h), the levels of blood urea nitrogen (BUN), creatinine (Cr), urine N-acetyl-β-D-glucosaminidase (NAG) and Cr were assayed. Kidney samples were harvested at 72h after I/R. The histological and pathologic changes of kidney were observed by electron microscope and light microscope.Results:Three kinds of IPO attenuated renal I/R injury and changes of urine NAG/Cr ratio and 24h Cr clearance in 24h,48h and 72h after I/R injury. The renal functional parameters of dogs were significantly different at 24h,48h and 72h after I/R injury. Compared with group 1, group 2 showed significant increases in BUN and Cr. However, IPO treatment significantly decreased BUN and Cr levels at 24h,48h and 72h after I/R (P<0.05).Conclusions:IPO exerts protective effects on renal (I/R) injury, the protection of which in the IPO of 15 seconds reperfusion/ischemia for 6 cycles was the most notable.PartⅡThe mechanism of ischemic postconditioning attenuates renal ischemic/reperfusion injuryObjective:To discuss the mechasim of ischemic postconditioning attenuates renal reperfusion/ischemiaMethods:Twenty five adult male mongrel dogs were randomly divided into five groups with 5 animals in each group:group 1, sham-operated group; group 2, I/R group; group 3,6x15 seconds IPO group, kidneys were subjected to six cycles of 15 seconds of reperfusion followed by 15 seconds of ischemia immediately after 60 minutes of ischemia; group 4,6×30 seconds IPO group, kidneys were subjected to six cycles of 30 seconds of reperfusion followed by 30 seconds of ischemia immediately after 60 minutes of ischemia; group 5,3×1 minute IPO group, kidneys were subjected to three cycles of 1 minute of reperfusion followed by 1 minute of ischemia immediately after 60 minutes of ischemia. Kidney samples were harvested at 72h after I/R. renal superoxide dismutase (SOD), malondialdehyde (MDA), 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 sham group, I/R resulted in renal dysfunction, decreased SOD levels, increased MDA and MPO levels, and increased apoptosis indices (P<0.05).Conclusions:IPO exerts protective effects on renal (I/R) injury. Its mechanisms may involve reduction of lipid peroxidation inflammation and cellular apoptosis.PartⅢIschemic postconditioning prevents chronic kidney fibrosis induced by ischemic reperfusion in a rat modelObjectives:I/R injury is the most common cause of renal dysfunction and it is also pivotal for renal fibrosis development. IPO is a phenomenon by which intermittent interruptions of blood flow in the early phase of reperfusion can protect organ from I/R injury. Previous study have shown that IPO can attenuate renal I/R injury in short term. In the present study, we investigated the effect of IPO on prevention of chronic kidney fibrosis.Materials and methods:Thirty six adult male Sprague-Dawley (200-250g) rats were randomly divided into three groups of 8 each:group sham operation(S); group I/R; group IPO. The IPO was induced by 6 cycles of reperfusion (15s) and ischemia (15s). Blood samples were collected at indicated reperfusion time point (2w). blood urea nitrogen (BUN) and creatinine (Cr) levels, and histological change were observed at 2 and 8 weeks after operation.α-smooth muscle actin(actin), transforming growth factor-β1(TGF-β1) and Smad2 were assessed by western blot and immunohisto-chemi story.Results:The levels of BUN and Cr were normal after 2 weeks in all groups. The pathological changes of kidney were similar in three groups by hematoxylin-eosin staining except mild lesion at renal tubule in I/R group. Campared with sham group, I/R caused the progression of interstitial fibrosis by Masson staining at 8 week(.P<0.05). a-actin,TGF-(31 and Smad2 protein levels were increased at 8 week in I/R group(P<0.05). However, IPO attenuated the above effects(P<0.05). Conclusions:I/R caused the progression of interstitial fibrosis. IPO exerts protective effects on renal (I/R) injury and prevents the progression of interstitial fibrosis in the long-term. |
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