摘要
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 。
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.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2003年第5期548-550,共3页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
浙江省跨世纪学术和技术带头人基金项目 (№ 992 0 86 )
温州市"551人才工程"培养基金项目(№ 980 18)
浙江省卫生厅科研基金项目(№ 98A0 87)
关键词
药理学
缺血-再灌注损伤
肝脏
乳酸脱氢酶
左旋精氨酸
氧自由基
一氧化氮
兔
pharmacology
hepatic ischemia reperfusion injury
lactic dehydrogenase
L Arginine
oxygen free radicals
nitric oxide
rabbits
