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已证明肾缺血后,内源性胺浓度升高至中毒水平。采取措施使尿液碱化,抑制谷酰胺酶,可保护肾免受缺血/再灌注损伤。为验证这一结论,Lenon选用体重250±50克的雄性大鼠30只,平均分成3组,于单侧肾温缺血前3小时静脉注射:Ⅰ.8.4%碳酸氢钠1ml;Ⅱ生理盐水1ml;Ⅲ.3%氯化钠2ml。Ⅰ、Ⅲ两组大鼠接受的钠当量相同。在制作单侧肾温缺血模型的同时,行对侧肾切除。分别手术前及恢复血流后1、3、7天测定血清肌酐。结果表明,Ⅰ组动物的肾功能得到明显保护,术后第3天肌酐水平升高至最高值:441±31μmol/L,而Ⅱ组为953±1gμmol/L。Ⅲ组为948
After renal ischemia has been proved, the endogenous amine concentration increased to poisoning levels. Take measures to alkalize the urine, inhibition of glutaminase, can protect the kidney from ischemia / reperfusion injury. To validate this conclusion, Lenon selected 30 male rats weighing 250 ± 50 g and divided them equally into 3 groups, intravenously 3 hours prior to unilateral renal warm ischemia: 1.8% sodium bicarbonate, 1 ml, Ⅱ normal saline 1ml; Ⅲ.3% sodium chloride 2ml. Rats in group I and III received the same sodium equivalent. In the production of unilateral renal warm ischemia model, contralateral nephrectomy. Serum creatinine was measured at 1, 3 and 7 days before surgery and after resuscitation. The results showed that the renal function of the animals in Group Ⅰ was obviously protected. The creatinine level increased to the highest level on Day 3 after operation: 441 ± 31μmol / L, while that of Group Ⅱ was 953 ± 1gμmol / L. Group Ⅲ was 948