梗阻性黄疸肾缺血再灌注损害及其机制的研究

目的：探讨梗阻性大鼠在短暂性肾缺血再灌注过程中肾功能改变与脂质过氧化反应及肾近曲小管上皮细胞内游离钙离子浓度变化之间的关系。方法：实验大鼠分为正常对照组（S组）、正常肾缺血再灌注组（SRI组）、梗阻性黄疸组（J组）、梗阻性黄疸肾缺血再灌注组（JRI组）。在胆道梗阻１周后行双侧肾动脉夹闭10min后放开，观察再灌注后0、4、12、24h等不同时相点观察肾功能的变化。采用钙离子荧光指示剂Fura-2/Am负载测定各组24h时相点肾近曲小管上皮细胞内游离钙离子浓度。结果：JRI组内生肌酐清除率随再灌注时间延长持续下降,J组及JRI组肾组织丙二醛水平明显升高同时超氧化物歧化酶含量下降。JRI组肾近曲小管上皮细胞内游离钙离子浓度显著升高。结论：在梗阻性黄疸状态下大鼠肾脏对缺血再灌注损伤的敏感性明显升高，缺血再灌注损伤可能与梗阻性黄疸术后急性肾功能衰竭的发生有关。氧自由基及钙超载参与了这一过程。

A study on mechanism of renal ischemic reperfusion injury in bile-duct ligated rats

Objective To illustrate relationship between the alteration of temporary RI on renal function of jaundiced rat and both the lipid perioxidation and the change of calcium concentration in proximal tubules.Methods Wistar rats were divided into 4 groups of sham operation group(S group), sham operation and renal RI group(SRI group), common bile duct ligation group(J group), common bile duct ligation and renal RI group(JRI group). One week after bile duct ligation, rat bilateral renal arteries were transiently occluded for 10 minutes.The variations renal function were observed at different time phases after renal reperfusion. Simultaneously, the calcium concentration in proximal tubules was measured. Results In JRI group, Ccr decreased progressively along with the prolongation of the duration of reperfusion. In J and JRI groups,the level of MDA in kidney increased while SOD decreased complicatedly. In JRI group the calcium concentration increased obviously.Conclusion Jaundiced rat was sensitite to RI. Thus,we believe that RI may be an important mechnism contributed to ARF after obstructive jaundice surgery. Lipid oxidative stress and calcium overload were involved in this process.