氯高铁血红素对早期糖尿病肾病大鼠肾脏的影响

目的:观察氯高铁血红素处理不同时期糖尿病大鼠肾脏结构和功能、核转录相关因子(Nrf-2)变化.方法:选取8周SD大鼠12只作为正常对照组(A组);对另36只SD大鼠采用高糖高脂联合链脲佐菌素法诱导建立糖尿病模型,建模后再分为糖尿病组(B组,n=17)和糖尿病+氯高铁血红素组(C组,n=17).检测8～14周大鼠体质量、血糖、24 h尿微量白蛋白,第10、14周提取大鼠肾组织匀浆,分析氧化应激产物丙二醛MDA含量,Western blotting检测肾脏HO-1、Nrf-2表达,PAS染色光镜下观察肾脏结构.结果:与正常对照组比较,B、C两组体质量均增高,而B组又显著高于C组(P<0.05).B、C两组血糖、24 h尿微量蛋白也显著高于正常对照组(P<0.05).不同时期比较显示,B、C组Nrf-2表达第14周均较第10周降低,C组Nrf-2均较B组升高(P<0.05),HO-1表达也呈现相同情况.MDA含量比较显示,第14周较第10周相比各组有显著升高;第10周时C组较B组低.结论:氯高铁血红素能改善早期糖尿病肾病大鼠肾脏结构和功能,并与抗氧化因子Nrf-2、HO-1表达有关.     

Imbalance of endogenous homocysteine and hydrogen sulfide metabolic pathway in essential hypertensive children

Background  Hypertension is a common disease of the cardiovascular system. So far, the pathogenesis of primary hypertension remains unclear. The elaboration of its pathogenesis is an important topic in the field which calls for urgent resolution. The aim of this study was to probe into the metabolic imbalance of homocysteine (Hcy) and hydrogen sulfide (H₂S) in children with essential hypertension, and its significance in the pathogenesis of essential hypertension.
Methods  Twenty-five children with essential hypertension and 30 healthy children with normal blood pressure were enrolled in the study. The medical history was investigated and a physical examination was conducted on the subjects. Plasma Hcy content was examined by fluorescence polarization immunoassay (FPIA). The plasma H₂S level was detected by a modified method with a sulfide electrode. Data were presented as mean±standard deviation. The t test was applied to the mean values of both groups. Pearson linear correlation analysis was applied to the plasma Hcy and H₂S as well as to the systolic pressure against the plasma H₂S/Hcy ratio.
Results  Plasma Hcy, an intermittent metabolite of the endogenous methionine pathway, was markedly increased but plasma H₂S, a final product of this pathway was significantly decreased in hypertensive cases when compared with normal subjects ((Hcy: (12.68±9.69) µmol/L vs (6.62±4.79) µmol/L (t=2.996, P<0.01); H₂S: (51.93±6.01) µmol/L vs (65.70±5.50) µmol/L) (t=-8.670, P<0.01)). The ratio of plasma H₂S/Hcy in children with hypertension was 5.83±2.91, while that of the control group was 11.60±3.30, and the difference is significant with a t=-6.610 and P<0.01. A negative correlation existed between plasma Hcy and H₂S concentrations, r=-0.379, P<0.05. And a negative correlation was found between systolic blood pressure and the plasma H₂S/Hcy ratio, r=-0.687, P<0.05.
Conclusion  There was a metabolic imbalance of homocysteine and hydrogen sulfide in essential hypertensive children.

     

氧化苦参碱通过抑制CHK1/2磷酸化改善糖尿病大鼠肾组织的纤维化和炎症

目的 探讨氧化苦参碱（OMT）抗炎抗纤维化是否是通过影响细胞周期检测点激酶1/2（CHK1/2）来发挥。方法 SD大鼠采用完全随机设计分为正常对照组（NC）、糖尿病模型组（DM）和氧化苦参碱治疗组（OMT）,6只/组,尾静脉注射链脲佐菌素（STZ）（55 mg/kg）复制糖尿病模型。HE、Masson染色观察病理组织形态学变化;免疫组织化学染色观察CHK1、CHK2、p-CHK1、p-CHK2的表达部位;ELISA检测肾组织上清中IL-6和IL-1β的含量;Western blot检测CHK1、CHK2、p-CHK1、p-CHK2、 Ⅲ型胶原（Col-Ⅲ）、Ⅳ型胶原（Col-Ⅳ）、纤维连接蛋白（FN）蛋白的表达水平;NRK-52E细胞按处理方式分为正常糖对照组（NG组）、高糖模型组（HG组）、正常糖用药组（NG+OMT组）、高糖用药组（HG+OMT组）、正常糖空载组（NG+con组）、正常糖敲低组（NG+siCHK1/2）、高糖空载组（HG+con组）、高糖敲低组（HG+siCHK1/2）,Western blot检测CHK1、CHK2、p-CHK1、p-CHK2、Col-Ⅲ、Col-Ⅳ、FN蛋白的表达水平。结果 OMT可降低大鼠血糖、血肌酐和24 h尿蛋白（P<0.05）;DM组大鼠肾脏已出现炎性细胞浸润和纤维化表型,OMT组有所改善;OMT有明显抗炎作用（P<0.05）;CHK1/2主要表达在肾小管胞浆及胞核,DM组CHK1/2磷酸化水平高于NC组、OMT组;大鼠肾组织和NRK-52E细胞中经OMT治疗后p-CHK1、p-CHK2、Col-Ⅲ、Col-Ⅳ、FN蛋白表达含量均明显下降（P<0.05）;敲低CHK1/2后p-CHK1/2、Col-Ⅲ、Col-Ⅳ、FN蛋白表达均明显下降（P<0.05）。结论 OMT在糖尿病大鼠肾脏中发挥抗炎、抗纤维化的作用机制可能是通过影响CHK1、CHK2的表达从而影响其磷酸化水平,减少下游炎症介质的释放,减轻细胞外基质的分泌和沉积。     

Multiple hemodynamic effects of endogenous hydrogen sulfide on central nervous system in rats

Background  Endogenous hydrogen sulfide is a new neuromodulator which takes part in the regulation of central nervous system physiology and diseases. Whether endogenous hydrogen sulfide in the central nervous system regulates cardiovascular activity is not known. In the present study, we observed the hemodynamic changes of hydrogen sulfide or its precursor by intracerebroventricular injection, and investigate the possible roles of endogenous digitalis like factors and sympathetic activity in the regulation.

Methods  Ninety-four Sprague-Dawley rats underwent a right cerebroventricular puncture, then the hydrogen sulfide saturation buffer or its precursor injected by intrcerebroventricular catheter. A heperin-filled catheter was inserted into the right femoral artery or into the left ventricle, and changes of blood pressure or cardiac function recorded by a Powerlab/4S instrument. Phentolamine or metoprolol were pre-injected to observe the possible role in autonomic nerve activity. After rats were sacrificed, plasma was collected and endogenous digitalis-like factors were measured with a commercial radioimmunoassay kit. The aortic, cardiac sarcolemmal vesicles were isolated and the activity of Na⁺-K⁺-ATPase was measured as ouabain-sensitive ATP hydrolysis under maximal velocity conditions by measuring the release of inorganic phosphate from ATP. Unpaired Student’s t test for two groups or analysis of variances (ANOVA) for multiple groups were used to compare the differences of the changes.

Results   Intracerebroventricular injection of hydrogen sulfide induced a transient hypotension, then dramatic hypertenive effects in a dose-dependent manner. Bolus injection of L-cysteine or beta-mercaptopyruvate also increased mean arterial pressure (P <0.01), whereas hydroxylamine-a cystathionine beta synthase inhibitor decreased the arterial pressure (P <0.01). Hydrogen sulfide and L-cysteine increased mean arterial pressure, left ventricular develop pressure and left-ventricle maximal rate of systolic and diastolic pressure; these functions were decreased by hydroxylamine (P <0.01). Glibenclamide (a K_ATP channel blocker) blocked the transient hypotensive effect, phentolamine (an alpha-adrenergic receptor blocker) blocked the hypertensive effect, and metoprolol (a selective beta 1 receptor blocker) blocked the positive inoptropic effect of central nervous system hydrogen sulfide. The endogenous digitalis-like factors in plasma were elevated (P <0.01) after treatment with L-cysteine, association with decreasing Na⁺-K⁺-ATPase activity in cardiac or aortic sarcolemmal vesicles (P <0.01). Hydroxylamine injection reduced the endogenous digitalis-like factors level in plasma association with increasing Na⁺-K⁺-ATPase activity in cardiac and aortic sarcolemmal vesicles.

Conclusion  Central nervous system endogenous hydrogen sulfide upregulated mean arterial pressure and cardiac systolic function by activation of sympathetic nerves or release of endogenous digitalis-like factors.

     

氯沙坦对STZ糖尿病大鼠肾脏超微结构的影响

目的 :观察血管紧张素受体拮抗剂氯沙坦对糖尿病大鼠肾脏超微结构的影响。方法 :雄性SD大鼠分为正常对照组 (NC)、糖尿病对照组 (DC)、糖尿病氯沙坦治疗组 (DL) ,治疗 12周 ,电镜观察各组肾脏超微结构的改变。结果 :DC组肾小球基底膜显著增厚 ,系膜和系膜细胞显著增生 ,DL组上述改变显著减轻。结论 :氯沙坦能够减轻或延缓糖尿病大鼠肾脏超微结构的改变 ,提示它能够对糖尿病肾脏产生一定的保护作用     

Effects of Atorvastatin on Warfarin-induced Aortic Medial Calcification and Systolic Blood Pressure in Rats

The effect of atorvastatin on warfarin-induced aortic medial calcification and systolic blood pressure （SBP） of rats induced by warfarin was studied. Thirty healthy and adult rats were randomly divided into Warfarin group （n=10）, Atorvastatin group （n=10） and normal control group （n=10）. Caudal arterial pressure of rats was measured once a week, and 4 weeks later, aorta was obtained. Elastic fiber, collagen fiber and calcium accumulation in tunica media of cells were measured by Von Kossa staining. The results showed that warfarin treatment led to elevation of systolic blood pressure and aortic medial calcification. The chronic treatment also increased collagen, but decreased elastin in the aorta. However, the atorvastatin treatment had adverse effects. It was concluded that treatment with atorvastatin presented evidence of blood pressure lowing and calcification reducing. These data demonstrate that atorvastatin protected aortic media from warfarin-induced calcification and elevation of systolic blood pressure.     

糖肾安改善糖尿病大鼠肾脏病变的作用

目的：研究中药复方糖肾安对糖尿病肾脏病变的改善作用。 方法：Wistar大鼠随机分为4组：对照组（CN）,糖尿病组（DM）,糖肾安处理的糖尿病组（DM+T）和氨基胍处理的糖尿病组（DM+A）。糖尿病大鼠用糖肾安（6 g•kg^-1）处理8周后,检查肾脏功能和结构的损害程度。 结果：与对照组大鼠比较,糖尿病大鼠血糖、血清肌酐（Scr）和尿素氮（BUN）及尿蛋白排泄量明显升高（P<0.01）。糖肾安处理未能明显降低糖尿病大鼠的血糖水平（P>0.05）,但Scr、BUN水平和尿蛋白排泄量明显下降（P<0.01）。给予糖肾安后明显降低糖尿病大鼠已升高的肾小球体积/体重比值。糖尿病大鼠肾小球系膜区PAS阳性染色物质沉积增多,肾小球基底膜呈节段性增厚,上皮细胞足突部分融合,糖肾安处理后这些形态改变明显改善。结论：糖肾安对糖尿病肾脏病变有明显改善作用。     

阿魏酸钠对糖尿病大鼠肾脏抗氧化酶的影响

目的：探讨阿魏酸钠（SF）对糖尿病大鼠肾脏抗氧化酶的影响。方法：对链脲佐菌素（STZ）诱导的糖尿病肾病大鼠灌胃给予SF110mg/kg/d，治疗8周，测定各组大鼠肾重/体重、血尿素氮(BUN)、血、尿肌酐、肌酐清除率(Ccr)、24h尿蛋白定量、血清果糖胺(FMN)、血清及肾脏超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、丙二醛（MDA）等。结果：糖尿病对照组大鼠肾重/体重、BUN、血肌酐（Scr）、Ccr、24h尿蛋白定量、血清FMN显著高于正常对照组，治疗组肾重/体重、BUN、Ccr、24h尿蛋白定量、血清FMN显著低于糖尿病组。糖尿病对照组大鼠肾脏和血清SOD、CAT活性显著低于正常对照组，MDA显著高于正常对照组，经SF治疗的糖尿病大鼠肾脏和血清SOD、CAT活性显著高于糖尿病对照组，MDA显著降低。结论：SF通过保护肾脏抗氧化酶，减轻氧化应激对糖尿病大鼠肾脏产生保护作用。     

Dynamic changes of renal cytosol glucocorticoid receptors in rats with passive Heymann nephritis

ＤｙｎａｍｉｃｃｈａｎｇｅｓｏｆｒｅｎａｌｃｙｔｏｓｏｌｇｌｕｃｏｃｏｒｔｉｃｏｉｄｒｅｃｅｐｔｏｒｓｉｎｒａｔｓｗｉｔｈｐａｓｓｉｖｅＨｅｙｍａｎｎｎｅｐｈｒｉｔｉｓ￥ＺｈａｏＤｏｎｇｂａｏ（赵东宝）；ＣｕｉＲｕｏｌａｎ（崔若兰）；ＴａｎＪｉｎｇｘ...     

促红细胞生成素对血管性痴呆大鼠神经干细胞增殖分化的影响

目的 探讨促红细胞生成素(erythropoietin,EPO)对血管性痴呆(vascular dementia,VD)大鼠神经干细胞(neural stem cell,NSC)增殖、分化及认知功能的影响.方法 SD大鼠45只,按随机数字表法分为对照组、VD组和治疗组;改良2-VO+硝普钠法建立VD大鼠模型;治疗组腹腔注射EPO;采用穿梭箱系统检测大鼠认知功能;免疫组化法检测神经干细胞增殖分化情况.结果 行为学测试:VD组大鼠AAR比率显著低于对照组(P<0.01);治疗组大鼠AAR比率显著高于VD组(P<0.01),但仍显著低于对照组(P<0.01).免疫组化结果:BrdU(5-Bromodeoxyuridine)标记阳性细胞随时间推移从海马颗粒下层(the subgranular zone,SGZ)向颗粒细胞层(granule cell layer,GCL)迁移.造模后1周,VD组BrdU标记阳性细胞数明显高于对照组(P<0.01),低于治疗组(P<0.01);治疗组大鼠BrdU+DCX(doublecortin)双标阳性细胞数明显高于VD组(P<0.01).造模后4周,各组BrdU标记阳性细胞数与造模后1周相比均有明显下降,其中VD组下降最明显.治疗组BrdU+NSE(neuron-specific-enolase)双标阳性细胞数明显多于VD组(P<0.01).各组大鼠各时相点BrdU标记阳性细胞数中神经元所占比例无统计学差异(P>0.05).结论 腹腔注射EPO可促进VD大鼠脑内NSC增殖,显著改善大鼠认知功能,但对NSC分化无明显影响.     

实验性糖尿病大鼠肾脏损害和脂质过氧化物水平的动态研究

动态观察实验性糖尿病大鼠于发病后２、４、６、１２、和１６周肾脏损害指标和肾脏脂质过氧化物（ＬＰＯ）水平的变化。结果表明，发病后各观察时间．或糖尿病大鼠２４ｈ尿Ａｌｂ、β２──ＭＧ排泄量和尿ＮＡＧ活性均明显增高，而２４ｈ尿ＴＨＰ排泄量显著降低，肾脏ＬＰＯ水平明显升高。其中尿ＮＡＧ活性、ＴＨＰ排泄量和肾脏ＬＰＯ水平均随病程延长而更趋明显。这些结果提示，在糖尿病早期除有肾小球功能损害外，肾小管也明显受损，过氧化损伤在糖尿病肾病发病中可能是重要因素之一。尿Ａｌｂ、β２──ＭＧ、ＴＨＰ含量和ＮＡＧ活性可作为糖尿病肾病早期肾损害的敏感指标。     

乌司他丁对糖尿病大鼠的肾脏保护作用及其机制

目的观察乌司他丁(UTI)对糖尿病大鼠肾脏的保护作用,并探讨其可能的机制。方法 Wistar大鼠30只,随机选10只为空白对照组(A组),余20只大鼠采用腹腔注射链脲佐菌素成功构建糖尿病模型后,随机分为糖尿病组(B组)及UTI干预组(C组),每组10只。C组每日腹腔注射UTI 40 000 IU/kg,A组及B组每日腹腔注射等量生理盐水。分别于第8周及第12周检测各组大鼠的空腹血糖(FPG)、24 h尿白蛋白、血肌酐(SCr)及尿肌酐,并计算内生肌酐清除率(Ccr);制备肾匀浆,并检测血清及肾匀浆丙二醛(MDA)、超氧化物歧化酶(SOD)、结缔组织生长因子(CTGF)、基质金属蛋白酶-9(MMP-9)及纤溶酶原激活物抑制剂-1(PAI-1)的含量。结果①B、C组FPG高于A组(P均<0.05),C组与B组间差异无统计学意义(P>0.05);②B、C组24 h尿白蛋白、SCr高于A组,C组低于B组(P均<0.05);③B、C组Ccr低于A组,C组高于B组(P均<0.05);④B、C组血清及肾匀浆MDA、CTGF及PAI-1含量均高于A组,C组低于B组(P均<0.05);⑤B、C组血清及肾匀浆SOD及MMP-9均低于A组,C组高于B组(P均<0.05)。结论 UTI对糖尿病大鼠肾功能具有保护作用,其机制可能与降低糖尿病大鼠MDA、CTGF及PAI-1表达、升高SOD及MMP-9表达,降低尿蛋白等因素有关。     

冬虫夏草降压作用实验研究

目的：观察冬早夏草对肾性高血压大鼠血压的影响。方法：体重为160－180g健康雄性Wistar大鼠随机分成三组：高血压（RH）组、高血压＋冬虫夏草（RH＋S）组及对照（C）组。RH组用经典的Goldblatt氏法复制。术后10天，RH＋S组用12．5％冬虫夏煎剂，按生药1g/kg,bid灌胃。20天后，用颈动脉直接插管法测定大鼠血压的变化并取出心脏称重。结果：冬虫夏草能明显降低肾性高血压大鼠的血压，并能逆转肾性高血压压时所发生的心肌肥大。结论：冬虫复草具有降低、逆转心肌肥大的作用。     

内皮素、一氧化氮在烧伤后肾脏血流调节中的作用

目的：研究内皮素（ＥＴ）、一氧化氮（ＮＯ）在烧伤后肾脏血流调节中的作用。方法：动态观察大鼠３０％Ⅲ度烧伤后血浆及是肾脏ＥＴ、ＮＯ含量及肾脏血流量变化，应用ＥＴ 体拮抗剂和外源性ＮＯ载体观察其对烧伤大鼠肾脏血流量的影响。结果：大鼠烧伤后肾脏血流量明显下降，伤后血浆及肾组织ＥＴ、ＮＯ含量升高，由于ＥＴ升主幅度盯对较大，ＥＴ／ＮＯ比值也显著增加，肾组织ＥＴ、ＥＴ／ＮＯ改变与肾脏血流量的降低呈显著负相关；     

腺苷三磷酸氯化镁对失血性休克大鼠血压和血酸性磷酸酶活性的影响

[目的 ]观察腺苷三磷酸 氯化镁对失血性休克大鼠血压及酸性磷酸酶活性的影响 .[方法 ]将 36只Wistar大鼠随机分为腺苷三磷酸 氯化镁组、腺苷三磷酸组、氯化镁组、对照组 .各组均用微量输液器从股静脉给药 .在实验的不同时期 ,以血浆酸性磷酸酶、平均动脉压做为指标探讨腺苷三磷酸 氯化镁抗大鼠失血性休克效应机理 .[结果 ]腺苷三磷酸 氯化镁抑制休克大鼠血酸性磷酸酶的活性 ,并对动脉血压有明显的回升作用 .[结论 ]腺苷三磷酸 氯化镁抗失血性休克效应明显 ,单用腺苷三磷酸或氯化镁效应不佳     

先天性与获得性孤立肾患儿血压及肾功能的差异分析

目的 探讨先天性与获得性孤立肾患儿在后期血压及肾功能上的差异。方法 该文为回顾性研究,按一定的纳入及排除标准,共选入55 例孤立肾患儿。其中先天性孤立肾37 例、获得性孤立肾18 例。记录孤立肾患儿在确诊时（T0）的血压及肾功能,包括肾小球滤过率、24 h 尿蛋白定量及动态血压监测。并于确诊后第14 年（T14）对患儿进行再次随访,并收集血压及肾功能数据。利用χ2 检验或Wilcoxon 检验比较不同时期两组患儿在血压及肾功能上的变化差异。结果 T0 与T14 比较,两组在肾小球效过滤及尿蛋白定量差异无统计学意义（P >0.05）。76.4%（42/55）的孤立肾患儿出现血压升高。其中获得性孤立肾患儿更易患高血压。先天性孤立肾患儿则更易引起前期高血压。组间比较,获得性孤立肾患儿较先天性孤立肾患儿出现血压增高的比例更高。结论 长期随访观察显示,孤立肾患儿肾功能无明显恶化趋势,可长期保持稳定。先天性孤立肾患儿与获得性孤立肾患儿在肾功能上差异无统计学意义。在血压变化上,无论何种病因,孤立肾患儿均会出现血压增高的趋势。获得性孤立肾患儿血压增高的风险较先天性孤立肾患儿高。此外,获得性孤立肾患儿中血压增高的形式以高血压为主,而先天性孤立肾患儿中血压增高的形式以前期高血压为主。     

Curcumin alters motor coordination but not total number of Purkinje cells in the cerebellum of adolescent male Wistar rats

OBJECTIVE: The present study aimed at investigating the effects of curcumin on the motor coordination and the estimate of the total number of cerebellar Purkinje cells of adolescent Wistar rats exposed to ethanol. METHODS: The total of 21 male Wistar rats aged 37 d old were divided into three groups, namely ethanol, ethanol-curcumin, and control groups. The ethanol group received 1.5 g/kg ethanol injected intraperitoneally and water given per oral; the ethanol-curcumin group received 1.5 g/kg ethanol injected intraperitoneally and curcumin extract given per oral; the control group received saline injection and oral water. The treatment was carried out daily for one month, after which the motor coordination performance of the rats was examined using revolving drum apparatus at test days 1, 8, and 15. The rats were finally sacrificed and the cerebellum of the rats was further processed for stereological analysis. The estimate of the total number of Purkinje cells was calculated using physical fractionator method. RESULTS: The ethanol-curcumin group performed better than both ethanol and control groups in the motor coordination ability at day 8 of testing (P< 0.01). No Purkinje cell loss was observed as a result of one month intraperitoneal injection of ethanol. CONCLUSION: Curcumin may exert beneficial effects on the motor coordination of adolescent rats exposed to ethanol via undetermined hormetic mechanisms.     

Effects of Chinese patent medicine Niaoduqing on adenineinduced chronic renal failure in rats

The authors made rat model of chronic renal failure by feeding the animals with foodcontaining 0.5 % adenine and treated with Niaoduqing(NDQ),a Chinese patent medicine,whichcomposed of Rhizoma Rhei,Radix Glycyrrhizae,Radix Paeoniae Alba,etc.The rats were divid-ed into four groups:model control,normal control;and two NDQ-treated groups with high andlow doses separately.The blood tests including urea nitrogen(BUN),serum creatinine(Scr),red blood cell(RBC),hemoglobin (Hb) hematocrit (HCT),sodium (Na),potassium (K),cal-cium(Ca)and phosphate(P)levels were performed atthe fourth week and the eighth week,thetime of sacrifice.The results showed that in the NDQ-treated groups the mean levels of BUN andScr were lower and the mean values of RBC,Hb and HCT,higher than those in the untreatedcontrol group.In the NDQ-treated groups,hyperphosphatemia and hypocalcemia of rats im-proved,the deposited crystals of adenine metabolite and the proliferation of fibroid tissue in kid-ney decreased.These findings indicate that NDQ can ameliorate the symptoms of chronic renalfailure and delay the progress of this disease.     

右美托咪啶预处理对大鼠肾缺血再灌注后肝肾抗氧化能力的影响

目的探究右美托咪啶（dexmedetomidine,DEX）预处理对大鼠肾缺血再灌注损伤后。肾及肝抗氧化能力的影响。方法90只雄性SD大鼠随机分为3组（n=30）,右美托咪啶预处理组（DEX组）,缺血再灌注组（IRI组）,假手术组（Sham组）。DEX组于建模前30min腹腔注射DEX（100μg／ks）,其余两组腹腔注射等量0．9％氯化钠注射液,建立肾缺血再灌注模型,再灌注后2h、8h、24h肝肾组织匀浆检测超氧化物歧化酶（serum levels of superoxide dismutase,SOD）、一氧化氮（nitric oxide,NO）、乳酸（lactate dehydrogenases,LD）、还原型谷胱甘肽（reduced glutathione,GSH）及总抗氧化能力（total antioxidant capacity,T—AOC）。结果与IRI组相比,DEX组肾匀浆SOD升高,总NO降低,T—AOC升高（P〈0．05）,LD再灌注8h后降低明显（P〈0．05）;肝SOD升高,总NO升高,T—AOC升高（P〈0．05）,LD再灌注8h、24h降低显著（P〈0．05）。结论右美托咪啶预处理可提高大鼠肾缺血再灌注后肾及肝的抗氧化能力,减少乳酸堆积。