兔肝缺血-再灌注损伤时乳酸脱氢酶活性的变化和左旋精氨酸的保护作用

目的 :探讨兔肝缺血 再灌注损伤 (HIRI)时乳酸脱氢酶 (LDH)活性的变化和左旋精氨酸 (L Arg)的保护作用及其机制。方法 :实验兔 2 1只 ,随机分为对照组、盐水组和L Arg组 ,每组 7只。制作肝缺血 再灌注损伤模型 ,观察血清及肝组织LDH活性、丙二醛 (MDA)浓度、超氧化物歧化酶 (SOD)活性、一氧化氮代谢产物 (NO-2 NO-3)水平的变化及L Arg对它们的影响。结果 :盐水组血清LDH活性进行性升高 (P <0 .0 1 ) ,肝组织内LDH、SOD活性和NO-2 NO-3水平明显下降 (P <0 .0 5 ,P <0 .0 1 ) ,而MDA含量显著增高 (P <0 .0 1 ) ;L Arg组变化不明显 ,与盐水组比较 ,血清及肝组织内LDH、SOD活性、MDA含量及NO-2 NO-3浓度 ,均有显著性差异 (P <0 .0 5或P <0 .0 1 )。结论 :L Arg可通过降低体内氧自由基水平、提高一氧化氮水平 ,对HIRI时LDH活性的异常改变起积极的保护作用

Change of lactic dehydrogenase activity and protection of L-arginine on ischemia-reperfusion injury in rabbits

AIM: To explore the changes of lactic dehydrogenase (LDH) activity and the protection of L arginine (L Arg) on ischemia reperfusion injury (HIRI) in rabbits. METHODS: Therabbits were randomly divided into three groups (n=7 in each): control group, 0.9 % NaCl group and L Arg group. Using a HIRI model, the activities of LDH and superoxide dismutase (SOD) in serum and hepatic tissue, the contents of malondialdehyde (MDA), and nitric oxide products (NO - 2/NO - 3) levels were measured in rabbits. RESULTS: In 0.9 % NaCl group, LDH activity increased progressivelyin serum (P< 0.01 ), and LDH, SOD activities and NO - 2/NO - 3 concentration decreased remarkably (P< 0.05 or P< 0.01 ), and MDA content increased significantly in hepatic tissue (P< 0.01 ). These changes did not show in L Arg group (P< 0.05 or P< 0.01 ). CONCLUSION: L Arg shows a protection on HIRI by decreasing oxygen free radical level and raising NO level.