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      백서에서 신 허혈성 손상에 미치는 칼슘 길항제의 효과 = Effects of Calcium Antagonists on Renal Ischemic Injury in Rat

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      https://www.riss.kr/link?id=A75165132

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      Renal ischemia is one of the most common causes of acute renal failure. Four factors related to the pathogenesis of acute renal failure are vasoconstriction, decreased glomerular filtration rate, tubular back leak of filtrate, and intratubular obstruc...

      Renal ischemia is one of the most common causes of acute renal failure. Four factors related to the pathogenesis of acute renal failure are vasoconstriction, decreased glomerular filtration rate, tubular back leak of filtrate, and intratubular obstruction. The cellular response to renal ischemic insults include decreased content of adenosine trihosphate, lipid peroxidation induced membrane degradation, alteration in cellular pH, and calcium or phospholipase induced mitochondrial dysfunction. Much attention has been given to the role of increased cellular calcium as a pathogenetic contributor to cell injury during ischemia.
      Author studied the protective effects of calcium antagonists on cellular injury during renal ischemia in rat. To investigate the protective role of these agents, author measured the amount of malondialdehyde(MDA) and the enzyme activities of free radical scarvengers-superoxide dismutase(SOD), catalase and glutathione peroxidase from non-pretreated group and calcium antagonists pretreated groups in control, ischemia and reflow subgroups.
      The results were summerized as follows:
      1) The amount of MDA in non-pretreated group was higher in the reflow compared with the control(<p<0.01). But, in all pretreated groups, there was no statistically difference in the amount of MDA.
      2) The SOD activity in non-pretreated group was lower in both the ischemia and the reflow compared with the control (P<0.05). But, in both verapamil and trifluoperazine-pretreated groups, there was no statistically difference in the SOD activity.
      3) Both catalase and glutathione peroxidase activities in non-pretreated group were lower in both the ischemia and the reflow compared with the control (P<0.05). But in all pretreated groups, there was no statically difference in both catalase and glutathione peroxidase activities. These results suggest that
      free radical mediated ischemic injury by renal artery clamp in rat can be protected by intraperitoneal pretreatment with calcium antagonists. As trifluoperazine has a protective effect in renal ischemia, the calcium activated calmodulin dependent enzyme may play a role in renal ischemic injury.

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