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。 Ulinastatine(UTI)是一种蛋白酶抑制剂，据报道有帮助 防止缺血和各种类型的休克；然而，其 这些保护作用的机制尚不完全清楚。我们有 目的：探讨尿路感染对大鼠肾缺血再灌注损伤的影响。 同时测量肾皮质和肾脏组织的氧分压 大鼠的延髓。主要实验方案为30分钟肾移植 缺血(通过夹住腹主动脉)，然后60分钟 再灌流。生理盐水组：生理盐水1ml/kg或尿路感染 UTI组在缺血前30min给予50000U/1ml/kg(UTI组)。在 NS组肾皮质和髓质对照PO2值为11.7 分别为+/-2.3和14.4+/-5.7毫米汞柱，而尿路感染 组分别为18.9+/-4.0和24.5+/-4.2 mm Hg。大脑皮层的氧分压 在缺血期间，两者的延髓都减少到不到2毫米汞柱 组。再灌注60min时，生理盐水组的氧分压为 未完全恢复(7.6+/-2.3和6.9+/-1.4毫米汞)，而 UTI组完全恢复到控制值(21.1 +/-4.8和25.5+/-2.1毫米汞柱)。这些数据表明， 缺血前应用UTI可增加肾皮质和 再灌流后延髓血氧分压。

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.