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Comparative Study
. 2011 Jul-Sep;16(3):108-13.
doi: 10.12659/aot.882002.

The effect of preservation solutions UW and EC on the expression of renin I, angiotensinogen and angiotensin I-converting enzyme genes in rat kidney

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Comparative Study

The effect of preservation solutions UW and EC on the expression of renin I, angiotensinogen and angiotensin I-converting enzyme genes in rat kidney

Tadeusz Sulikowski et al. Ann Transplant. 2011 Jul-Sep.

Abstract

Background: Ischemia/reperfusion injury in organ transplantation is a multifactor process that may lead to delayed graft function (DGF), and has a significant impact on short- and long-term graft survival. The activation of the renin-angiotensin system may be important in the pathophysiology of DGF. Preservation solutions are thought to diminish the ischemic injury, and appropriate choice of the solution should contribute to improved graft function and better prognosis for graft survival. The aim of this study was to examine the effect of preservation solutions UW and EC on the expression of renin I, angiotensinogen and angiotensin I-converting enzyme genes in rat kidney.

Material/methods: The study was carried out on Wistar rat kidneys divided into 3 groups: kidneys perfused with 0.9% NaCl (control group), with UW preservation solution, and with EC preservation solution. We investigated the expressions of renin I, angiotensinogen- and angiotensin I-converting enzyme genes in kidneys perfused with EC and UW solutions after 12 min (minutes) and 24 h (hours) of cold ischemia and 30 min of warm ischemia.

Results: The perfusion with UW and EC solution caused an increase of renin I, angiotensinogen and angiotensin I-converting enzyme genes expression in kidneys. This increase was enhanced in kidneys perfused with UW solution in comparison with kidneys perfused with EC solution. The 24 h preservation with UW solution resulted in a decrease of renin-angiotensin activity increased in cold ischemia.

Conclusions: UW preservation of 24 h decreased renin-angiotensin system activity activated in cold ischemia but not in warm ischemia.

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