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| 1 | 一氧化氮在胃食管反流病发病机制中的作用显示文摘目的 探讨一氧化氮(NO)在胃食管反流病(GERD)发病机制中的作用。 方法 应用PC polygraf HR高分辨多通道测压系统检测GERD患者的食管下括约肌压力(LESP)、食管下括约肌长度(LESL)及食管远端蠕动幅度等动力参数;应用Digitrapper MKⅢ动态食管pH监测仪检测其24h食管内pH各项参数;应用硝酸还原酶法测定血清NO含量。 结果 与对照组比较,Savary Miller Ⅰ,Ⅱ,Ⅲ级GERD患者的LESP均显著降低(分别为1.1kPa±0.1kPa,1.1kPa±0.06kPa,1.0kPa±0.08kPa,P均<0.01);Savary Miller Ⅰ,Ⅱ,Ⅲ级GERD患者的食管下段蠕动幅度也均显著降低(分别为7.7kPa±1.1kPa,7.2kPa±1.3kPa,6.9kPa±1.2kPa,P均<0.01);GERD患者的食管内24h pH值明显高于对照组;其血清NO含量也显著高于对照组。 结论 内源性NO可能参与GERD的致病机制。 | 黄颖秋 王昕 李骢 刘丽 | 2000 | 世界华人消化杂志2000，8，3： | 17 |
| 2 | Effects of tumor necrosis factor,endothelin and nitric oxide on hyperdynamic circulation of rats with acute and chronic portal hypertension显示文摘AIM:To evaluate the effect of tumor necrosis factor (TNF),endothelin (ET) and nitric oxide (NO) on hyperdynamic circulation (HC) of rats with acute and chronic portal hypertension (PHT).METHODS: Chronic portal hypertension was induced in Wistar rats by injection of carbon tetrachloride. After two weeks of cirrhosis formation, L-NMMA (25mg/kg) was injected into one group of cirrhotic rats via femoral vein and the experiment was begun immediately. Another group of cirrhotic rats was injected with anti-rat TNFα (300mg/kg) via abdominal cavity twice within 48h and the experiment was performed 24h after the second injection. The blood concentrations of TNFα, ET-1 and NO in portal vein and the nitric oxide synthase (NOS) activity in hepatic tissue were determined pre-and post-injection of anti-rat TNFα or LNMMA. Stroke volume (SV), cardiac output (CO), portal pressure (PP), superior mesenteric artery blood flow (SMA flow) and lilac artery blood flow (IAflow) were measured simultaneously. Acute portal hypertension was established in Wistar rats by partial portal-vein ligation (PVL). The parameters mentioned above were determined at 0.5h,24h, 48h, 72h and 120h after PVL. After the formation of stable PHT, the PVL rats were injected with anti-rat TNFα or L-NMMA according to different groups, the parameters mentioned above were also determined.RESULTS:In cirrhotic rats, the blood levels of TNFα, NO in portal vein and the liver NOS activity were significantly increased (P<0.05) while the blood level of ET-1 was not statistically different (P>0.05) from the control animals(477.67±83.81pg/mL vs 48.87±32.79pg/mL, 278.41±20.11μmol/L vs 113.28±14.51μmol/L, 1.81±0.06μ/mg.prot vs 0.87±0.03μ/mg.prot and 14.33±4.42pg/mL vs8.72±0.79pg/mL, respectively). After injection of anti-rat TNFα,the blood level of TNFα was lower than that in controls (15.17±18.79pg/mL vs 48.87±32.79pg/mL). The blood level of NO and the liver NOS activity were significantly decreased, but still higher than those of the controls. The blood level of ET-1 was not significantly changed. PP,SV,CO, SMAflow and IAflow were ameliorated. After injection of L-NMMA, the blood level of NO and the liver NOS activity were recovered to those of the controls. PP and CO were also recovered to those of the controls. SV, SMAflow and IAflow were ameliorated. In PVL rats, the blood levels of TNFα NO in portal vein and the liver NOS activity were gradually increased and reached the highest levels at 48h after PVL. The blood level of ET-1 among different staged animals was not significantly different from the control animals. PP among different staged animals (2.4±0.18kPa at 0.5h, 1.56±0.08kPa at 24h, 1.74±0.1kPa at 48h,2.38±0.05 kPa at 72h, 2.39±0.16 kPa at 120h) was significantly higher than that in controls (0.9±0.16kPa). After injection of anti-rat TNFα in 72h PVL rats, the blood level of TNFα was lower than that in controls (14±14pg/mL vs 48.87±32.79pg/mL). The blood level of NO and the liver NOS activity were significantly decreased, but still higher than those of the controls. The blood level of ET-1 was not significantly changed. PP was decreased from 2.38±0.05kPa to 1.68±0.12kPa, but significantly higher than that in controls. SV, CO, SMAflow and IAflow were ameliorated.After injection of L-NMMA in 72h PVL rats, the blood level of NO and the liver NOS activity were recovered to those of the controls. PP, SV, CO, SMAflow and IAflow were also recovered to those of the controls.CONCLUSION:NO plays a critical role in the development and maintenance of HC in acute PHT and is a key factor for maintenance of HC in chronic PHT. TNFα may not participate in the hemodynamic changes of HC directly, while play an indirect role by inducing the production of NO through activating NOS. No evidence that circulating ET-1 plays a role in both models of portal hypertension has been found. | Ji-JianWang Gen-WuGao Ren-ZhongGao Chang-AnLiu XiongDing Zhen-XiangYao | 2004 | World Journal of Gastroenterology2004，10，5： | 14 |
| 3 | 肝硬化胰岛素抵抗及血清生长激素水平的研究显示文摘目的:研究肝硬化患者胰岛素抵抗和血清生长激素(GH)水平的关系.方法:选择肝硬化患者40例,按Child-Pugh分级将其分为ChildA级(16例)、B级(13例)和C级(11例),正常对照组22例,用放射免疫法测定空腹血清胰岛素和GH水平,并计算胰岛素敏感性指数(ISI);同时分析Child-Pugh分级与血胰岛素、ISI和GH的关系.结果:肝硬化患者的血清胰岛素(17.8±7.2U/L)和GH水平(3.7±2.2μg/L)较正常对照组(分别为10.1±3.4U/L和1.9±0.9μg/L)显著升高(分别是P<0.05和P<0.01),并随着Child-PughA,B,C分级的升高而升高;而肝硬化患者ISI显著低于正常对照组(0.017±0.010vs0.025±0.014,P<0.05),并随着Child-PughA,B,C分级的升高而降低;肝硬化C级的空腹血清胰岛素(23.6±10.1U/L)和GH水平(4.7±2.6μg/L)显著高于肝硬化A级(分别为13.8±4.5U/L和3.1±1.4μg/L)而肝硬化C级的ISI(0.012±0.007)显著低于肝硬化A级(0.019±0.011);肝硬化患者的Child-Pugh积分与胰岛素水平呈正相关(r=0.428,P<0.01),与GH水平呈正相关(r=0.376,P<0.05),与ISI呈负相关(r=-0.333,P<0.05);ISI与GH呈负相关(r=0.388,P<0.05);合并腹水、肝性脑病和肝癌的患者的血清胰岛素、GH水平较合并上消化道出血的患者显著升高(P<0.05).结论:肝硬化患者存在着高胰岛素血症、胰岛素抵抗和高GH症,他们均与肝功能的损伤程度有关. | 张卫卫 王学清 李岩 | 2002 | 世界华人消化杂志2002，10，10： | 12 |
| 4 | Study of T-lymphocyte subsets,nitric oxide,hexosamine and Helicobacter pylori infection in patients with chronic gastric diseases显示文摘INTRODUCTIONChronic gastritis(CG)and peptic ulcer(PU)arefrequently-occurring diseases.It is now well recognizedthat Helicobacter pylori(Hp)is a major factor that leadsto CG and PU.In order to study the relationshipamong T lymphocyte subsets,NO,Hexosamine and | Zhang H Jiang SL Yao XX | 2000 | World Journal of Gastroenterology2000，6，4： | 10 |
| 5 | Plasma endothelin in patients with endotoxemia and dynamic comparison between vasoconstrictor and vasodilator in cirrhotic patients显示文摘INTRODUCTIONPortal hypertension is a common clinical syndromecharacterized by an abnormal increase in portalblood to the systemic circulation, bypassing theliver. Recent studies have reported that humoralsubstances play an important role in thepathogenesis of portal hypertension, either byincreasing vascular resistance at both theintrahepatic and porto-collateral sites or affectingsplanchnic vasodilation with a concomitant increasein parto-collateral blood flow[1-6] | Feng Liu1 Ji Xin Li2, Chun Mei Li2 Xi Sheng Leng2 1Department of General Surgery, the Fifth Affiliated Hospital, Harbin Medical University, Harbin 150036, Heilongjiang Province, China2Department of General Surgery, People’s Hospital, Medical University, Beijing 100044, China | 2001 | World Journal of Gastroenterology2001，7，1： | 8 |
| 6 | Effects of estradiol on liver estrogen receptor-α and its mRNA expression in hepatic fibrosis in rats显示文摘AIM:Estradiol treatment regulates estrogen receptor (ER) level in normal rat liver.However,little information is available concerning the role of estrogen in regulating liver ER in hepatic fibrosis in rats.The present study was conducted to determine whether estradiol treatment in CCl4-induced liver fibrosis of female and ovariectomized rats altered liver ERα and its mRNA expression,and to investigate the possible mechanisms.METHODS:Seventy female rats were divided into seven groups with ten rats in each. The ovariectomy groups were initiated with ovariectomies and the sham operation groups were initiated with just sham operations.The CCl4 toxic fibrosis groups received 400mL/L CCI4 subcutaneously at a dose of 2 mL/kg twice weekly.Estrogen groups were treated subcutaneously with estradiol 1mg/kg, the normal control group and an ovariectomy group received injection of peanut oil vehicle twice weekly.At the end of 8 weeks,all the rats were killed to detect their serum and hepatic indicators,their hepatic collagen content, and liver ER and ER mRNA expression.RESULTS: Estradiol treatment in both ovariectomy and sham ovariectomy groups reduced liver levels of ALT (from 658±220nkat/L to 311±146nkat/L and 540±252nkat/L to 314±163nkat/L,P<0.05) and AST (from 697±240nkat/L to 321±121nkat/L and 631±268nkat/L to 302±153nkat/L,P<0.05),increased serum nitric oxide (NO) level (from 53.7±17.1μmol/L to 93.3±4.2μmol/L and 55.3±3.1μmol/Lto 87.5±23.6μmol/L, P<0.05) and hepatic nitric oxide synthase (NOS) activity (from 1.73±0.71KU/g to 2.49±1.20KU/g and 1.65±0.46KU/g to 2.68±1.17KU/g, P<0.05),diminished the accumulation of hepatic collagen,decreased centrolobular necrotic areas as well as the inflammatory reaction in rats subjected to CCl4. The positive signal of ER and ER mRNA distributed in parenchymal and non-parenchymal hepatic cells,especially near the hepatic centrolobular and periportal areas.Ovariectomy decreased ER level (from 10.2±3.2 to 4.3±1.3) and ER mRNA expression (from 12.8±2.1 to 10.9±1.3) significantly (P<0.05). Hepatic ER and ER mRNA concentrations were elevated after treatment with estradiol in both ovariectomy (15.8±2.4, 20.8±3.1) and sham ovariectomy(18.7±3.8, 23.1±3.7) fibrotic groups (P | Jun-WangXu JunGong Xin-MingChang Jin-YanLuo LeiDong AiJia Gui-PingXu | 2004 | World Journal of Gastroenterology2004，10，2： | 8 |
| 7 | Expression of TNF-α and VEGF in the esophagus of portal hypertensive rats显示文摘AIM: To investigate the expression of tumor necrosis factor-alpha (TNF-α) and vascular endothelial growth factor (VEGF) in the development of esophageal varices in portal hypertensive rats.METHODS: Thirty male Sprague-Dawley (SD) rats in the model group in which a two-stage ligation of portal vein plus ligation of the left adrenal vein was performed, were divided into three subgroups (M7, M14, and M21) in which the rats were kiued on the seventh day, the 14th d and the 21 d after the complete portal ligation. Thirty male SD rats, which underwent the sham operation in the control group, were also separated into three subgroups (C7, C14and C21) corresponding to the models. The expression of TNF-α and VEGF in the esophagus of all the six subgroups of rats were measured with immunohistochemical SP technique.RESULTS: The portal pressure in the three model subgroups was significantly higher than that in the corresponding control subgroups (23.82±1.83 vs 11.61±0.86 cmH2O,20.90±3.27 vs 11.43±1.55 cmH2O and 20.68±2.27 vs 11.87±0.79 cmH2O respectively, P<0.01), as well as the number (9.3±1.6 vs 5.1±0.8, 11.1±0.8 vs 5.4±1.3 and 11.7±1.5 vs 5.2±1.1 respectively, P<0.01) and the total vascular area (78 972.6±3 527.8 vs 12 993.5±4 994.8μm2, 107 207.5±4 6461.4 vs 11 862.6±5 423.2 μm2 and 110 241.4±49 262.2 vs 11 973.7±3 968.5 μm2 respectively,P<0.01) of submucosal veins in esophagus. Compared to the corresponding controls, the expression of TNF-α and VEGF in M21 was significantly higher (2.23±0.30 vs 1.13±0.28and 1.65±0.38 vs 0.56±0.30 for TNF-α and VEGF respectively, P <0.01), whereas there was no difference in M7 (1.14±0.38 vs 1.06±0.27 and 0.67±0.35 vs 0.50±0.24for TNF-α and VEGF respectively, P>0.05) and M14 (1.20±0.25vs 1.04±0.26 and 0.65±0.18 vs0.53±0.25 for TNF-α and VEGF respectively, P>0.05). And the expression of TNF-α and VEGF in M21 was significantly higher than that in M7(2.23±0.30 vs 1.14±0.38 and 1.65±0.38 vs 0.67±0.35 for TNF-α and VEGF respectively, P<0.01) and M14 (2.23±0.30vs 1.20±0.25 and 1.65±0.38 vs 0.65±0.18 for TNF-α and VEGF respectively, P<0.01), but there was no difference between M7 and M14 (1.14±0.38 vs 1.20±0.25 and 0.67±0.35vs 0.65±0.18 for TNF-α and VEGF respectively, P >0.05).CONCLUSION: In the development of esophageal varices in portal hypertensive rats, increased TNF-α and VEGF may be not an early event, and probably play a role in weakening the esophageal wall and the rupture of esophageal varices. | Zhao-HuiYin Xun-YangLiu Rang-LangHuang Shu-PingRen | 2005 | World Journal of Gastroenterology2005，11，8： | 7 |
| 8 | iNOS/NO体系在慢性肝炎及肝硬化患者中的表达显示文摘目的:探讨内源性NO在慢性病毒性肝炎-肝硬化发展进程中的作用.方法:采用硝酸还原酶法比色测定外周静脉及门静脉血浆中iNOS活性,并用免疫组织化学和RT-PCR方法观察肝组织iNOS蛋白及RNA的表达.结果:在慢性肝炎患者及肝硬化患者门静脉血与外周血中iNOS活性与对照组相比均明显升高(F=102.793,25.052,P<0.01),且门静脉血iNOS活性增高更为明显.慢性肝炎组及肝硬化组中iNOS蛋白的灰阶值均低于正常对照组(F=46.796,P<0.05),表明iNOS表达增强.慢性肝炎组、肝硬化组iNOSmRNA的表达均分别显著高于正常对照组(F=26.832,P<0.01),且随着肝脏病变的加重表达逐渐增加.结论:iNOS/NO体系在慢性肝炎-肝硬化发生发展中起着保持血管舒张状态的重要作用. | 李睿 张宁 赵瑾 徐丽红 黎永军 刘芳 陈卫刚 | 2010 | 世界华人消化杂志2010，18，7： | 7 |
| 9 | 内皮素、一氧化氮与肝硬化显示文摘肝硬化是各种慢性肝病发展到晚期的一种病理改变,肝功能损害、门静脉高压是其突出的表现。近年来,血管活性物质对肝脏疾病影响的研究已成为一个热点,特别是内皮素(ET)和一氧化氮(NO)。ET和NO是血管内皮细胞产生的生物调节因子,ET是由内皮细胞产生的一种多肽,具有缩血管和扩血管作用,而NO为一种强有力的血管内皮细胞舒张因子,具有强烈扩张血管作用。实验证实ET和NO与肝硬化的发生密切相关。 | 陈卫刚 李睿 褚云香 郑勇 | 2009 | 医学综述2009，15，22： | 6 |
| 10 | 门脉注入扩血管药物对鼠门脉高压的作用显示文摘目的研究门脉和下腔静脉注入扩血管药物对门脉和全身血流动力学的影响,寻找药物治疗门脉高压症的合适途径及药物。方法采用CCl_4诱发的鼠肝硬变门脉高压模型56只,随机平均分为8组,哌唑嗪(PRZ),维拉帕米(VER),DDPH和硝酸甘油(NG)分别经下腔静脉和门静脉注入,比较药物经此两种途径给药对门脉压(PVP),平均动脉压(MAP)和心率(HR)的影响。结果四种药物经下腔静脉注入和门静脉注入均可使PVP和MAP下降。其中PRZ,NG,DDPH门脉给药使PVP分别平均下降18.6%,13.9%,12.7%,而经下腔静脉给药PVP下降分别为10.5%,7.2%,2.3%,均有显著性差异(P<0.01)。VER经门脉和下腔静脉给药PVP下降分别为7.0%和2.6%,无统计学差别。PRZ,NG,VER,DDPH下腔静脉给药使MAP分别平均下降24.1%,15.8%,14.1%,10.4%,明显高于其经门脉给药,后者分别平均下降12.4%,6.1%,3.8%,5.7%,差异均有显著性。VER下腔静脉给药使HR平均下降7.6%,而门脉给药HR平均仅下降1.0%,有显著性差异。PRZ,DDPH和NG经两种途径对HR影响无显著性差别。DDPH门脉给药维持降压时间最久。结论门脉给药是扩血管药物治疗门脉高压症的理想途径,DDPH是较适宜的门脉给药途径降门脉压药物。 | 吴汉平 冯敢生 梁惠民 | 2001 | 世界华人消化杂志2001，9，2： | 6 |
| 11 | Regulatory effects of electro-acupuncture at Zusanfi on ir-SP content in rat pituitary gland and peripheral blood and their immunity显示文摘INTRODUCTIONIt has been reported in many studies that electro-acupuncture(EA)can positively regulate erythrocyticimmunity and T-lymphocytic subgroups.Nevertheless,its mechanism remains to be explored.In thepresent study,a multi-group,multi-stepped and multi-indexed observation was conducted on the effects of EA | Wei Gao Yu Xin Huang Hong Chen Da Yong Song Qin Li Wang Department of Gastroenterology Medical Affair Office,Tangdu Hospital,4th Military Medical University,Xi’an 710038,Shanxi Province,China Department of Gastroenterology,Chinese PLA General Hospital of Guangzhou Command Area,Guangzhou 510210,Guangdong Province,China | 2000 | World Journal of Gastroenterology2000，6，4： | 5 |
| 12 | Study on the mechanism of regulation on peritoneal lymphatic stomata with Chinese herbal medicine显示文摘AIM: To study the mechanism of Chinese herbal medicine(CHM), the prescription consists of Radix SalviaeMiltiorrhizae , Radix Codonopsitis Pilosulae , RhizornaAtractylodis Alba and Rhizoma Alismatis, LeonurusHeterophyllus Sweet, etc ) on the regulation of theperitoneal lymphatic stomata and the ascites drainage.METHODS: The mouse model of live fibrosis wasestablished with the application of intragastric installationsof carbon tetrachloride once every three days; scanningelectron microscope and computer image processing wereused to detect the area and the distributive density of theperitoneal lymphatic stomata; and the concentrations ofurinary ion and NO in the serum were measured analyzed inthe experiment.RESULTS: Two different doses of CHM could significantlyincrease the area of the peritoneal lymphatic stomata,promote its distribution density and enhance the arainage ofurinary ion such as sodium, potassium and chlorine.Meanwhile, the NO concentration of two different doses ofCHM groups was 133.52 ± 23.57μmol/L, and 137.2 ±26.79μnol/L respectively. In comparison with the controland model groups ( 48.36 ± 6.83μmol/L, and 35.22 ±8.94μmol/L, P < 0.01 ), there existed significantly markeddifference, this made it clear that Chinese herbal medicinecould induce high endogenous NO concentration. The effectof Chinese herbal medicine on the peritoneal lymphaticstomata and the drainage of urinary ion was altered byadding NO donor (sodium nitropurruside, SNP) or NOsynthase (NOS) inhibitor (N(G)-monomethyl-L-arginine, L-NMMA) to the peritoneal cavity.CONCLUSION: There existed correlations between high NOconcentration and enlargement of the peritoneal lymphaticstomata, which result in enhanced drainage of ascites.These data supported the hypothesis that Chinese herbalmedicine could regulate the peritoneal lymphatic stomata byaccelerating the synthesis and release of endogenous NO. | Shi-PingDing Ji-ChengLi 等 | 2002 | World Journal of Gastroenterology2002，8，1： | 5 |
| 13 | 肝硬化不同病期ET-1,NO对离体肝脏血流动力学的调节作用显示文摘目的:在肝硬化(LC)形成的不同病期、离体状态下动态研究内皮素-1(ET-1)、一氧化氮(NO)对肝循环血流动力学调节作用的变化规律。方法:皮下注射四氯化碳菜籽油溶液,乙醇代饮水,制备大鼠LC模型。根据造模不同时间,结合肝组织病理改变及有无腹水对LC进行分期,将造模第9周末定为LC早期(E-LC),14wk末定为LC晚期(L-LC),采用离体肝灌流技术动态研究ET-1,NO对肝血流动力学调节作用的变化规律。结果:门脉灌注L-NAME,L-LC组、E-LC组和对照组PP和Phv均无明显改变(P>0.05),门脉灌注ET-1可明显增加大鼠的PP(P<0.01),L-LC组PP增加幅度大于E-LC组(P<0.01)和对照组(P<0.01),给予L-NAME+ET-1与单独给予ET-1相比,PP进一步升高(P<0.05),LC大鼠PP增加幅度大于正常大鼠(P<0.01),但L-LC组与E-LC组PP增加幅度无明显差异(P>0.05)。结论:ET-1是导致肝内血流阻力增加的主要原因,ET-1可促进NO合成,此作用在LC时增强,NO代偿不足,且随着LC病情发展NO代偿能力进一步下降,导致ET-1、NO间作用失衡是引起LC门脉压增高的重要原因,在本病的治疗上可考虑应用ET受体拮抗剂或NO供体增加肝内NO合成,来抑制ET-1的作用,降低肝内阻力。 | 姚冬梅 姚希贤 杨川杰 冯志杰 房红梅 高军萍 | 2003 | 世界华人消化杂志2003，11，6： | 5 |
| 14 | 一氧化氮在大鼠梗阻性黄疸继发肝功能损伤中的作用显示文摘目的:探讨一氧化氮(NO)在梗阻性黄疸合并肝功能障碍中的作用. 方法:将56只Wistar大鼠随机分成假手术对照组和胆总管结扎组(实验组).应用胶原酶灌注法分离肝细胞并进行培养; 用白介素-1β(IL-1β)等细胞因子处理培养的肝细胞,应用Griess法和Western印迹分析法检测两组NO及诱导型一氧化氮合酶(iNOS)的产生;应用高效液相色谱法(HPLC)检测两组肝细胞5’三磷酸腺苷(ATP)的合成;应用酶法检测两组肝细胞酮体含量并计算酮体比率(乙酰乙酸盐/β-羟基丁酸盐) (KBR). 结果:实验组NO产生量明显高于对照组(207.99μmoL/L vs 78.57 μmoL/L P<0.01);NO的产生与IL-1β作用时间和作用剂量有关;实验组和对照组的iNOS产生量在蛋白水平没有差异;IL-1β降低了实验组培养肝细胞的ATP含量(15.94 nmoL/106 cells vs 20.21 nmoL/106cells,P<0.05), 对照组改变不明显;IL-1β降低了两组的KBR,实验组降低程度大于对照组;一氧化氮合酶(NOS)抑制剂NG-甲基- L-精氨酸(L-NMMA)抑制了NO的产生,使降低的肝细胞ATP含量、KBR得以恢复. 结论:梗阻性黄疸能够促进肝细胞产生NO,导致肝功能障碍.L-NMMA可以缓解由于大量NO导致的ATP合成障碍及KBR下降.对NO产生的调节可能会成为预防及治疗梗阻性黄疸继发肝功能损害的有效方法. | 涂巍 智迎辉 郭仁宣 | 2004 | 世界华人消化杂志2004，12，4： | 4 |
| 15 | 门奇静脉断流术对门脉高压症一氧化氮及氧自由基的影响显示文摘目的:探讨NO系统、OFR系统对门脉高压症(PHT)的影响及门奇静脉断流术的作用。 方法:门脉高压症患者19例,肝功能A级9例,B级10例;正常对照组15例。术前、术后d3晨空腹抽静脉血应用硝酸盐还原酶法测定NO,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD),比色法测定一氧化氮和酶(NOS),硫代巴比妥酸(TBA)法测定丙二醛(MDA)。 结果:肝硬化PHT患者术前血清NO(μmol·L^(-1))含量、NOS活性(kU·L^(-1))A级分别为63.8±10.7,26.3±7.9,B级分别为79.2±14.8,36.7±9.0,较正常对照组32.7±6.2,12.5±4.1显著升高(p<0.01);术前肝功能B级NO、NOS较A级显著升高(p<0.01);门奇静脉断流术后3dNO、NOSA级分别为40.2±9.4,16.9±5.3,B级分别为58.7±12,26.6±6.5与术前比均有显著降低(p<0.05,p<0.01),但仍高于正常对照组(p<0.05,p<0.01);且门奇静脉断流术后肝功能A级的NO、NOS的下降幅度分别为37.0%,35.8%较B级的25.8%,26.3%明显。肝硬化PHT患者术前血清SOD活性(kNU·L^(-1))A、 B级分别为70.5±16.7,53.3±11.1均较正常对照组119.1±20.1显著降低(p<0.01);而PHT患者术前血情MDA含量(μmol·L^(-1))A、B级分别为21.4±4.8,32.6±6.3则显著高于对照组6.7±2.0(p<0.01);术前肝功能B级SOD、MDA与A级比也有显著性差异(p<0.01,p<0. | 姚常柏 吴硕东 夏振龙 | 2002 | 世界华人消化杂志2002，10，1： | 4 |
| 16 | 功能性消化不良患者血清一氧化氮含量与食管动力变化特征研究显示文摘目的 探讨一氧化氮 (NO)在功能性消化不良 (FD)患者食管动力变化中的作用。方法 5 8例FD患者和 19名健康受试者纳入本研究 ,应用PCPolygraphHR动力监测系统测定FD患者食管压力 ;应用硝酸还原酶法测定血清NO含量。结果 FD患者食管下段平均蠕动波幅显著低于对照组 (7 12± 1.35kPavs 13.2 6± 2 .36kPa ,P <0 .0 1) ,而双峰波的病理性蠕动发生率则显著高于正常对照组 (48.3%vs 10 .5 % ,P <0 .0 1)。FD组血清NO含量显著高于对照组 (99.7± 17.5 μmoL/Lvs 72 .4± 15 .2 3μmoL/L ,P <0 .0 1)。结论 功能性消化不良患者存在食管运动功能异常 。 | 王春虹 黄颖秋 | 2002 | 胃肠病学和肝病学杂志2002，11，4： | 3 |
| 17 | 肝性脑病大鼠中缝核群内5-羟色胺表达的研究显示文摘目的观察肝性脑病大鼠和正常大鼠脑中缝背核5-羟色胺的表达;探讨中缝核神经元的形态学改变及5-羟色胺在肝性脑病发病机制中的作用。方法雄性大鼠35只,建立肝性脑病模型后,通过免疫细胞化学染色方法观察中缝核5-羟色胺阳性神经元的变化,并用图像分析仪对中缝核5-羟色胺能神经元进行光密度及体积测定,进行定量分析并与正常组相比较。结果肝性脑病大鼠脑内5-羟色胺神经元比对照组大鼠光密度值显著增高;直径显著减小。结论 5-羟色胺表达发生改变,提示这种神经递质参与了肝性脑病神经元的损伤,对肝性脑病大鼠神经系统有一定的影响。 | 蔡书景 郭秀英 | 2013 | 现代中西医结合杂志2013，22，22： | 2 |
| 18 | 小儿肝硬化门脉高压症的研究新进展显示文摘肝硬化门静脉高压症是由门脉系统血流受阻和(或)血流量增加,导致门脉系统内压力升高,所引发的一系列血流动力学改变和临床综合征,其是儿童中发病率较低的严重并发症,其发病率国内外尚无确切报道,国内外报道男女发病比例约为2:1[1,2]. | 张金山(综述) 李龙(审校) | 2010 | 中华小儿外科杂志2010，，9： | 2 |
| 19 | 进行性系统性硬化症患者血清一氧化氮含量和食管动力变化特征的研究显示文摘背景:进行性系统性硬化症(PSS)患者多伴有食管动力功能障碍,而一氧化氮(N0)在PSS食管动力异常发病机制中的作用尚不清楚。目的:探讨NO在PSS食管动力异常发病机制中的作用。方法:12例PSS患者和12名健康志愿者纳入本研究。应用硝酸还原酶法测定受试者的血清NO含量;应用PC polygraph HR高分辨多通道测压系统检测食管下括约肌(LES)压力(LESP)、LES长度(LESL)和食管远端蠕动幅度等动力参数;应用Digitrapper MKⅢ动态pH监测仪监测24 h食管内pH等参数。结果:PSS患者的血清NO含量显著高于对照组(106.47μmol/L±18.21μmol/L对82.32μmol/L±15.30μmol/L,P<0.01),LESP显著低于对照组(1.21 kPa±O.11 kPa对2.38 kPa±0.16 kPa,P<0.05),食管远端蠕动幅度亦显著低于对照组(5.18 kPa±1.04 kPa对14.93 kPa±2.12 kPa,P<0.01),75%的PSS患者有一过性LES松弛(TLESR)。PSS患者24 h食管内pH<4的发生频率显著高于对照组。结论:内源性NO可能参与了PSS食管动力异常的发病机制。 | 黄颖秋 王昕 刘丽 | 2002 | 胃肠病学2002，7，6： | 1 |
| 20 | 肝硬化门脉高压大鼠组织中一氧化氮合酶分布及其活性研究显示文摘目的探讨一氧化氮(NO)与门脉高压症的关系.方法采用四氯化碳(CCl4)复制肝硬化模型成功后,用NADPH黄递酶组织化学染色方法观察一氧化氮合酶(NOS)在肝组织、腹主动脉中的分布,并比较其活性.结果NADPH黄递酶组织化学染色法证实NOS主要分布于肝细胞、肝血管内皮、腹主动脉内皮及血管平滑肌细胞中,实验组总体NOS活性高于对照组.结论NO参与门脉高压及其高动力循环状态的发生. | 彭必村 袁文清 张明亮 | 2002 | 医学临床研究2002，19，1X： | 1 |
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