小儿肾病综合征血清一氧化氮与氧自由基的作用

一氧化氮（ＮＯ）是一种活性很强的自由基，在疾病的发生发展过程中起重要作用。我们通过测定４６例小儿肾病综合征（ＮＳ）患儿血清ＮＯ水平、丙二醛（ＭＤＡ）及超氧化物歧化酶（ＳＯＤ）含量的变化，对ＮＯ与氧自由基的相互关系在肾病综合征发病机制中的作用进行初步探讨，以便指导临床治疗。 一、材料与方法 １．观察对象：小儿 ＮＳ ４６例，男 ３２例，女１４例，年龄１岁６月～１３岁，均符合全国小儿肾脏病协作组制定的标准。病例入选条件：（１）未用过糖皮质激素、维生素Ｃ及维生素Ｅ治疗；（２）不伴有任何感染性疾病；（３）原…     

内源性一氧化氮对大鼠急性坏死性胰腺炎的胰腺保护作用

目的 探讨内源性一氧化氮（ＮＯ）对大鼠实验性急性坏死性胰腺炎的作用及其与胰腺血流的关系。方法 经胰胆管内注射５％牛磺胆酸钠溶液（１ｍｌ／ｋｇ）制成Ｗｉｓｔａｒ大鼠急性坏死性胰腺炎模型。以Ｌ－硝基精氨酸（Ｌ－ＮＮＡ）为内源性ＮＯ的阻断剂,观察内源性ＮＯ对胰腺损伤程度的影响;不同时相胰腺炎大鼠胰腺血流量的改变;内源性ＮＯ对损伤状态下大鼠胰腺血流量的影响。结果 经胰胆管注射牛磺胆酸钠可造成大鼠胰腺组织明     

二巯基丁二酸对肾组织损伤的保护作用

二巯基丁二酸对肾组织损伤的保护作用任青ＨａｒｖｅｙＣ．ＧｏｎｉｃｋＡｒｔｈｕｒＨ．Ｃｏｈｅｎ本实验是用高盐饮食将高血压基因鼠造成与人类高血压相似的模型，然后观察二巯基丁二酸（２，３－ｄｉｍｅｒｃａｐｔｏｓｕｃｃｉｎｉｃａｃｉｄＤＭＳＡ）对该鼠的肾脏及...     

急性胰腺炎大鼠氧自由基的变化与肺损伤的关系

近年来 ,氧自由基等炎性介质已被证实在急性胰腺炎(ＡＰ)的发病机制中起着重要的作用。本研究重点探讨ＡＰ大鼠氧自由基水平的变化与肺损伤的关系。材料与方法一、动物与分组ＳＤ大鼠 48只 ,体重 180～ 2 5 0ｇ ,雌雄各半 ,由苏州医学院动物中心提供。随机分为对照组和ＡＰ组各 2 4只。二、动物模型的制备参照Ｃｈｅｔｔｙ法 ,术前大鼠禁食 2 4ｈ ,不禁水。用 2 5 %戊巴比妥钠腹腔内注射麻醉 (0 1ｍｌ/ 10 0ｇ体重 )。腹正中切口入腹 ,提起胃 ,切开胃窦部置入塑料管 (长 4ｃｍ、直径 3ｍｍ)至十二指肠 ,以 3 0线将十二指肠肠管结扎于塑料…     

表皮生长因子对急性胰腺炎大鼠胰腺的保护作用

目的探讨表皮生长因子(EGF)对急性胰腺炎(AP)大鼠胰腺保护作用的机理。方法SD大鼠72只,随机均分为3组:对照组、AP组及AP-EGF组。AP-EGF组动物在诱导致AP模型后皮下注射EGF0.1μg/g体重,其余2组动物皮下注射相同体积的生理盐水。各组动物分别于术后6、12及24h剖杀取材(每个时相8只动物),经心脏取血4ml,其中2ml采用全自动生化分析仪检测血清淀粉酶,其余用于检测血浆中丙二醛(MDA)含量;以干纱布吸沾腹水,腹水量为浸满腹水的纱布重量与干纱布重量之差;各时相剖腹作大体观察,切取相同部位的胰腺组织5g检测其MDA含量,并观测胰腺组织病理学改变和细胞凋亡。结果AP-EGF组动物胰腺病理损伤较AP组轻;术后12及24h,AP-EGF组动物腹水量显著低于AP组〔(4.53±1.29)g vs(6.58±1.47)g、(7.64±1.85)g vs(11.96±2.13)g,P<0.05,P<0.01〕,AP-EGF组动物血清淀粉酶也显著低于AP组〔(142.0±8.3)U/L vs(187.9±10.4)U/L、(194.3±10.4)U/L vs(253.3±8.6)U/L,P<0.05,P<0.01〕;术后24h,AP-EGF组动物血浆中MDA含量为(2.34±0.23)μmol/L,胰腺组织中MDA含量为(5.21±1.46)μmol/g,均显著低于AP组的(3.15±0.38)μmol/L和(7.68±1.63)μmol/L,P<0.05,P<0.01;术后各时相,AP-EGF组动物胰腺细胞凋亡指数显著高于AP组〔(16.22±3.53)%vs(7.35±1.04)%、(11.67±2.40)%vs(4.81±0.86)%、(6.38±1.42)%vs(1.97±0.21)%,P<0.01〕。结论EGF能减轻AP时大鼠胰腺的病理损伤,迅速恢复血清淀粉酶正常活性,降低AP大鼠血浆及胰腺组织中MDA含量,通过诱导AP时腺体细胞的凋亡发挥对胰腺的保护作用。     

一氧化氮在重症急性胰腺炎细菌移位中的保护作用

以往的研究表明，重症急性胰腺炎（ＳＡＰ）时肠道细菌可移到其他脏器，导致继发感染［１］。近年来一氧化氮（ＮＯ）在急性胰腺炎中的作用日益受到人们的重视，研究表明ＮＯ对轻、重型急性胰腺炎均有保护作用［２］，而其对细菌移位的影响未见报道。为此我们观察了ＫＯ供体Ｌ－Ａｒｇ和ＮＯ合成酶抑制剂Ｌ－ＮＡＭＥ对大鼠ＳＡＰ细菌移位的影响，为防治其继发感染提供理论和实验依据。材料和方法１．动物ＳＤ大鼠４８只，雌雄不限，体重２００～２５０ｇ。２．ＳＡＰ模型的建立大鼠乙醚浅麻醉后，严格无菌操作，取上腹正中切口，将胃提出腹…     

急性胰腺炎大鼠肝,肾超微结构的改变及其与氧自由基的关系

用制作十二指肠闭袢的方法复制大鼠急性胰腺炎模型，于术后８ｈ、１６ｈ和２４观察急性胰腺炎大鼠肝、肾超微结构的改变；同时测定肝、肾组织的超氧化物歧化酶（ＳＯＤ）、丙二醛（ＭＤＡ）及血浆ＭＤＡ的水平。结果提示氧自由基及其引发的脂质过氧化反应参与了急性胰腺炎并发的肝、肾损害的病理过程。     

内毒素型损伤与一氧化氮的关系及山莨菪碱对其影响

目的：探讨内毒素型肺损伤与一氧化氮的关系及山莨菪碱对其影响。方法：３０只ＳＤ大鼠随机分成对照组、ＥＴ组、ＥＴ＋山莨菪碱组，静脉注射内毒素（２００ug/kg）造成急性 肺损伤。结果：４h后血浆和肺组织匀浆中ＮＯ２/ＮＯ３含量和丙二醛（ＭＤＡ）含量、肺系数、肺含水量、肺干湿相对密度均显著升高，与对照组比较差异有显著性（Ｐ＜０．０５或Ｐ＜０．０１），人毒素后５min、２h静脉注射山莨菪碱（５mg/kg）可明显减轻内毒素     

内源性一氧化氮对急性胰腺炎大鼠胰腺微血管通透性的影响

目的 探讨内源性一氧化氮（NO）对急性坏死性胰腺炎大鼠胰腺炎大鼠胰腺微血管通透性的影响。方法 以5%牛磺胆酸钠溶液胰胆管注射（1ml/kg）制成大鼠急性坏死性胰腺炎模型,以工具药L-硝基精氧酸（L-NNA）和内源性NO的阻断Evans Blue的漏出代表微血管的通透性,观察内源性NO对胰腺组织损伤程度、胰腺内Evans Blue漏出等的影响。结果 牛磺胆酸钠胆管注射造成大鼠胰腺组织明显坏死和炎性细胞浸润,以及血清淀粉酶浓度升高、胰腺湿/干重比率产加和明显的胰腺组织内Evans Blue积聚。以L-NNA（12.5mg/kg）阻断内源性NO后,胰腺组织坏死和炎性细胞浸润进一步加重,并使血清淀粉酶浓度升高,胰腺湿/干重比率增加,Evans Blue的漏出率也较之单纯胰腺炎组大鼠明显增加。结论 内源性NO具有胰腺保护作用,其保护机制可能与维持胰腺微血管的完整性有关。     

一氧化氮对大鼠移植胰腺再灌注损伤的保护作用

目的　探讨一氧化氮 (NO)对大鼠移植胰腺再灌注损伤的保护作用。方法　应用同系大鼠异位全胰十二指肠移植模型 ,大鼠移植术前和术后 5min静脉注射L 精氨酸 (L Arg ,2 0 0mg/kg)和N 硝基 L 精氨酸甲酯 (L NAME ,10mg/kg) ,移植术后 1～ 72h经腹主动脉取血测定大鼠空腹血糖、血清中脂肪酶、淀粉酶及中性粒细胞化学趋化性细胞因子 (CINC)含量 ,测定移植胰腺组织中NO含量、CINCmRNA的表达及髓过氧化酶 (MPO)活性 ,并进行组织学观察。结果　移植胰腺组织中NO含量L Arg组 >对照组 >L NAME组 ;CINC在再灌注后 3h出现峰值 ,L Arg组为(7.66± 1.5 3 ) μg/L ,L NAME组为 (3 4.18± 3 .12 ) μg/L ,对照组为 (2 6.3 1± 2 .0 1) μg/L ,差异有显著性 (P <0 .0 5 ) ;移植物中CINCmRNA于再灌注后 3h表达最强 ,L Arg组表达水平明显低于L NAME组和对照组 ;L Arg组胰小叶间质水肿和胰小叶内中性粒细胞浸润较轻。 结论　外源性应用L Arg或L NAME能够分别增加或减少胰腺组织NO含量 ,NO能抑制CINC的升高及CINCmRNA的表达 ,抑制中性粒细胞浸润 ,对移植胰腺再灌注损伤起保护作用。     

Effect of oxygen free radicals on the rat pancreas in vivo]

Many reports concerning the involvement of active oxygen free radicals in the pathogenesis and progression of acute pancreatitis have been published. In this study, the direct toxic effect of active oxygen free radicals on the rat pancreas was evaluated in vivo. Superoxide anions, generated via the xanthine/xanthine oxidase (X/XO) system, and hydrogen peroxide (H2O2) were used. After continuous arterial injection of X/XO into the celiac artery hemorrhage and extensive edema developed. However, additional continuous injection of superoxide dismutase (SOD) into the external jugular vein completely suppressed the hemorrhage and relieved the edema. When hydrogen peroxide (100 microM/Kg/hour) was injected continuously through the celiac artery made hemorrhage and edema were recognized in the pancreas, both of which were suppressed by continuous injection of catalase (10 mg/Kg/hour) or gabexate mesilate (10 mg/Kg/hour) into the external jugular vein. The amylase and lipase levels in the intraperitoneal fluid rose to more than 10 times the preoperative values 5 hours after drug administration. These levels were lowered to 2 times the preoperative values by the continuous venous injection of SOD or catalase (which are specific scavengers of superoxide anions or hydrogen peroxide, respectively) or by gabexate mesilate. On the other hand, serum amylase and lipase levels remained almost constant throughout the entire experiment. Thus, the administration of active oxygen free radicals caused acute pancreatitis, which was suppressed by the systemic administration of specific scavengers for each free radical. Active oxygen free radicals were shown to have a direct, toxic effect on the pancreas.     

Oxygen free radicals regulate splanchnic nitric oxide synthesis and blood flow

This study examines the hypothesis that oxygen radicals down-regulate splanchnic nitric oxide synthesis and contribute to splanchnic vasoconstriction following hemorrhage/reperfusion injury. Anesthetized rats underwent placement of flow probes around the superior mesenteric artery and abdominal aorta. Animals were bled to 30 mmHg for 30 min, reperfused without or with superoxide dismutase, an oxygen radical scavenger, 15 min before reperfusion and compared with sham-treated rats. Animals were sequentially teated with the nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester (l-NAME) at 10 mg/kg and l-arginine, a nitric oxide precursor, at 200 mg/kg or 400 mg/kg. l-NAME increased systemic pressure and decreased superior mesenteric artery blood flow whereas l-arginine decreased arterial pressure and increased superior mesenteric artery blood flow in the sham animals. Hemorrhage/reperfusion injury attenuated the pressure and superior mesenteric artery blood flow changes following l-NAME and l-arginine dosing, which was reversed by superoxide dismutase treatment. These data suggest that oxygen free radicals regulate splanchnic nitric oxide synthesis, thus contributing to splanchnic vasoconstriction following hemorrhage/ reperfusion injury.     

The roles of free oxygen radicals, nitric oxide, and endothelin in caustic injury of rat esophagus

Purpose

The authors aimed to find out the roles of free oxygen radicals, nitric oxide (NO), and endothelin (ET) in caustic injury of rat esophagus.

Methods

Forty-five Wistar albino rats were used to form 6 groups. The study groups are summarized as 1, sham (S; n = 7); 2, sham + l-arginine (SA; n = 7); 3, sham + l-NAME (SN; n = 7); 4, injury (I; n = 8); 5, injury + l-arginine (IA; n = 8); 6, injury + l-NAME (IN; n = 8). Normal saline in the sham groups and 50% NaOH in the caustic injury groups were administered to the distal esophagus. Free oxygen radicals and NO were detected by chemiluminescence from tissue samples, and they were correlated with histologic examinations. Tissue ET was measured also with immunohistochemistry.

Results

The injury was verified histologically. Free oxygen radical levels were found to be increased as well as NO and ET with the caustic injury (P < .05). l-arginine caused a histologic increase in the injury that was close to statistical significance (P = .08). l-NAME showed no significant effect.

Conclusions

Free radicals, NO, and ET increase in the early phase of caustic esophageal injury. Understanding their early interactions during the caustic injury may help in future therapeutic strategies.     

烫伤大鼠心肌细胞一氧化氮生成对心肌的保护作用

目的了解氨基胍对烫伤大鼠心肌的影响。方法将72只Wistar大鼠随机分为烫伤组、氨基胍组。2组大鼠均造成30％TBSAⅢ度烫伤后常规补液，氨基胍组伤前20min腹腔内注射氨基胍（40mg／kg）。于伤前及伤后1、3、6、12、24h取大鼠动脉血检测血清中心肌肌钙蛋白I（cTnI）浓度、一氧化氮（NO）浓度，另取心肌组织测定NO浓度；观察氨基胍组、烫伤组伤后6h大鼠的心功能水平。结果伤后3h烫伤组大鼠血清NO浓度[（59．6±5．4）μmol／L]明显高于伤前[（24．6±0．8）μmoL／L，P〈0．01]，6h达峰值，24h明显回落，均明显高于氨基胍组（P〈0．01）；心肌组织NO浓度的变化趋势同上。与烫伤组比较，氨基胍组伤后各时相点cTnI浓度明显升高。与烫伤组伤后6h比较，氨基胍组大鼠该时相点的心功能抑制加重。结论氨基胍可抑制NO生成，加重了烫伤大鼠的心肌损害并使其心功能下降，提示NO对烫伤后早期心肌可能具有保护效应。     

The effect of carbon dioxide pneumoretroperitoneum on free oxygen radicals in rabbit retroperitoneoscopy model

The aim of this study was to investigate the possible effects of carbon dioxide (CO2) pneumoretroperitoneum on free oxygen radicals in the kidney. Twelve male New Zealand rabbits were divided into 2 equal groups; group 1; control operation group (retroperitoneal space preparation without CO2 insufflation) and group 2; study group (10-12 mm Hg pneumoretroperitoneum for 3 hours with CO2). At the end of the procedure, laparotomy was performed to harvest ipsilateral and contralateral kidney in both groups after three hours. Kidney tissues were homogenized and were assayed for malondialdehyde (MDA), protein carbonyls (for protein oxidation), and reduced glutathione (GSH). Ipsilateral and contralateral kidney tissue levels of the MDA, protein carbonyls and GSH were not different in both the study and the control group (P > 0.05 for all comparisions). Corresponding ipsilateral and contralateral tissue levels of the markers, MDA and protein carbonyls were found to be significantly different in the study group as compared with the control group (P < 0.05 for the four comparisons mentioned). However, neither the ipsilateral nor the contralateral tissue levels of the marker GSH showed statistically relevant difference when the study group was compared with the control group. Oxidative stress was identified as a component of CO2 pneumoretroperitoneum-induced kidney injury using an animal model of retroperitoneoscopy. Oxidative stress is likely to contribute to the impairment of renal function after retroperitoneoscopy using a 10 mm-12 mm Hg CO2 pneumoretroperitoneum.