BLOOD OXYGEN LEVEL DEPENDENT (BOLD) MR IMAGING & BRAIN OXYGEN TENSION

肾缺血是急性肾功能衰竭的主要原因。 乌司他汀（UTI），一种蛋白酶抑制剂，据报道， 防止缺血和各种类型的休克;然而， 这些保护作用的机制尚不完全清楚。 我们有 研究UTI对肾缺血和再灌注的影响， 同时测量肾皮质中的组织pO 2， 大鼠延髓。 主要实验方案为30 min肾性 缺血（通过夹闭腹主动脉），随后60分钟 再灌注 NS组给予0.9%NaCl 1 ml/kg，UTI组给予0.9%NaCl 1 ml/kg UTI组于缺血前30 min给予50000 U/1 ml/kg。 在 NS组肾皮质和髓质的对照pO 2值分别为11.7 分别为+/- 2.3和14.4 +/- 5.7 mmHg，而UTI中的患者 组分别为18.9 ± 4.0和24.5 ± 4.2 mmHg。 皮层的pO 2 在缺血期间， 组 再灌注60 min时，NS组pO 2值为： 未完全恢复（7.6 +/- 2.3和6.9 +/-1.4 mmHg），而 UTI组则完全恢复到对照组水平（21.1 +/-4.8和25.5 +/-2.1 mmHg）。 这些数据表明 缺血前给予UTI增加了肾皮质和 再灌注后延髓pO 2。

Renal ischemia is a major cause of acute renal failure. Ulinastatine (UTI), a protease inhibitor, has been reported to help protect against ischemia and various types of shock; however, its mechanism for these protective effects is not fully known. We have investigated the effects of UTI on renal ischemia and reperfusion by measuring the tissue pO2 simultaneously in the renal cortex and medulla in rats. The principal experimental protocol was 30 min renal ischemia (by clamping the abdominal aorta) followed by 60 min reperfusion. Treatments were 0.9%NaCl 1ml/kg (NS group) or UTI 50000U/1ml/kg (UTI group) administered 30 min before ischemia. In the NS group, the control pO2 values of renal cortex and medulla were 11.7 +/- 2.3 and 14.4 +/- 5.7 mmHg respectively, whereas those in the UTI group were 18.9 +/- 4.0 and 24.5 +/- 4.2 mmHg. The pO2 of the cortex and medulla decreased to less than 2 mmHg during ischemia in both groups. At 60 min after reperfusion, the pO2 values in NS group were not fully restored (7.6 +/- 2.3 and 6.9 +/-1.4 mmHg), whereas those in the UTI group were completely restored to the control value (21.1 +/-4.8 and 25.5 +/- 2.1 mmHg) . These data indicate that administration of UTI before ischemia increases the renal cortical and medullary pO2 after reperfusion.