اثر آماده سازی بافتی بر تغییرات مقدار ویتامین E در شرایط ایسکمی-پرفیوژن مجدد در کلیه موش صحرایی

 During kidney and other organ transplantation, the organ to be transplanted, must inevitably remain out of the body with little or no blood perfusion at all for a long period of time (ischemia). These events have been suggested to cause the formation of oxygen- derived free radicals (OFR). Reperfusion (reintroduction of blood flow) will further exacerbate the initial damage caused by the ischemic insult and may result in the production of free radicals. The aim of this study was to investigate whether induction of brief periods of renal artery occlusion (ischemic pre‌conditioning, IPC) can provide protection from the effects of a subsequent period of ischemia and reperfusion (IR) in the rat kidney.Materials and Methods: In this regard, 28 white, male rats were randomly and equally divided into four groups: Control (sham- operated), IPC alone, IR alone (30 min ischemia followed by 10 min reperfusion), and IPC- IR. Preconditioning involved the sequential clamping of the right renal artery for 5 min and declamping for 5 min for a total of 3 cycles. To demonstrate the effectiveness of IPC regimen, vitamin E as an endogenous antioxidant and an index of lipid peroxidation was measured by HPLC after its extraction from right renal venous plasma and right renal tissue.Results: Results of this study showed that the amount of vitamin E of renal tissue and venous plasma in the IR group had a significant decrease when compared to the control group (P< 0.0001). Whereas the amount of this vitamin in both renal tissue and venous plasma of the IPC- IR group was significantly higher than that in the IR group (P< 0.0001), but did not show any significant difference with the control group.Conclusion: In this study, preconditioning method prevented the reduction of the endogenous antioxidant (Vit. E) in encountering the following sustained ischemic insult. Therefore, we suggest that ischemic preconditioning can be used to protect the Vit. E level of kidney from its subsequent decrease by ischemia and reperfusion.