Serviddio Gaetano, Romano Antonino Davide, Gesualdo Loreto, Tamborra Rosanna, Di Palma Anna Maria, Rollo Tiziana, Altomare Emanuele, Vendemiale Gianluigi
Division of Nephrology, Department of Biomedical Sciences, University of Foggia Viale Pinto, 71100 Foggia, Italy.
Nephrol Dial Transplant. 2008 May;23(5):1504-12. doi: 10.1093/ndt/gfm779. Epub 2008 Feb 19.
Several recent studies have shown that a brief ischaemia applied during the onset of reperfusion (postconditioning) is cardioprotective in different animal models. The potential application of postconditioning to organs different from the heart, i.e. kidney, is not available and is investigated in the present study. We also tested the hypothesis that mitochondria play a central role in renal protection during reperfusion.
Wistar rats were subjected to left nephrectomy and 90-min right kidney occlusion. In controls, the blood flow was restored without intervention. In postconditioned rats, complete reperfusion was preceded by 3 min, 6 min and 12 min of reperfusion in a consecutive sequence, each separated by 5 min of reocclusion. Animals were studied for 48 h. Mitochondrial respiratory chain function, rate of hydroperoxide production and carbonyl proteins were measured at the end of postconditioning and 24 h and 48 h after reperfusion.
BUN and creatinine significantly decreased in the postconditioning group as compared to control rats. Mitochondrial respiratory function was significantly impaired in control rats, mainly at the level of Complex II. Postconditioning significantly reduced this mitochondria impairment. The rate of mitochondrial peroxide production was higher in the control group than in the protected group at the end of postconditioning reperfusion. Moreover, mitochondrial protein oxidation was significantly higher in control rats than in the postconditioning group at the end of reperfusion. Conclusions. In the present study, postconditioning reduced renal functional injury and reduces mitochondria respiratory chain impairment, mitochondria peroxide production and protein damage.
最近的几项研究表明，在再灌注开始时进行短暂缺血（后适应）在不同动物模型中具有心脏保护作用。后适应在不同于心脏的器官（即肾脏）中的潜在应用尚未见报道，本研究对此进行了探究。我们还检验了线粒体在再灌注期间的肾脏保护中起核心作用这一假说。
对Wistar大鼠进行左肾切除术并对右肾进行90分钟的阻断。对照组在不进行干预的情况下恢复血流。在后适应组大鼠中，在完全再灌注之前，依次进行3分钟、6分钟和12分钟的再灌注，每次再灌注之间间隔5分钟的再阻断。对动物进行48小时的观察。在后适应结束时以及再灌注后24小时和48小时测量线粒体呼吸链功能、过氧化氢产生速率和羰基蛋白。
与对照大鼠相比，后适应组的血尿素氮和肌酐显著降低。对照大鼠的线粒体呼吸功能显著受损，主要在复合物II水平。后适应显著减轻了这种线粒体损伤。在后适应再灌注结束时，对照组的线粒体过氧化物产生速率高于保护组。此外，在再灌注结束时，对照大鼠的线粒体蛋白氧化显著高于后适应组。结论。在本研究中，后适应减少了肾功能损伤，并减轻了线粒体呼吸链损伤、线粒体过氧化物产生和蛋白损伤。
