Smeesters C, Corman J, Fassi J C, Giroux L, St-Louis G, Jean G, Daloze P
Can J Surg. 1983 Mar;26(2):175-7, 180.
An experimental model of canine normothermic renal ischemia was used to determine whether lysosomal urinary enzyme excretion reflects the extent of ischemic cellular injury, as assessed by subsequent renal function (serum creatinine level) and morphologic changes. The value of a lysosomal membrane-stabilizing agent (methylprednisolone) in protecting kidneys from ischemic damage by preventing lysosomal enzyme release was assessed. Results showed conclusively that urinary enzyme activities of beta-galactosidase and N-acetyl-beta-glucosaminidase are valuable indicators of renal cellular damage and functional outcome after ischemic injury, and that methylprednisolone at a dose of 30 mg/kg, given intravenously 1 hour before a 1-hour period of normothermic ischemia, protects the kidney both biologically and morphologically, by reducing the excretion of lysosomal enzymes after revascularization.
采用犬常温肾缺血实验模型，以确定溶酶体尿酶排泄是否反映缺血性细胞损伤程度，这通过后续肾功能（血清肌酐水平）和形态学变化进行评估。评估了一种溶酶体膜稳定剂（甲基泼尼松龙）通过防止溶酶体酶释放来保护肾脏免受缺血损伤的价值。结果确凿地表明，β-半乳糖苷酶和N-乙酰-β-氨基葡萄糖苷酶的尿酶活性是缺血性损伤后肾细胞损伤和功能结果的重要指标，并且在常温缺血1小时前1小时静脉注射30mg/kg剂量的甲基泼尼松龙，通过减少血管再通后溶酶体酶的排泄，在生物学和形态学上保护肾脏。
