|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | 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 |
| 2 | 内毒素血症致肝脏损伤显示文摘 | 夏晨梅 张顺财 | 2008 | 肝脏2008，13，2： | 9 |
| 3 | 阻塞性黄疸与肝细胞能量变化显示文摘阻塞性黄疸可以通过多种机制造成肝细胞损伤,近年来围绕阻塞性黄疸对肝细胞损伤机制的研究已取得很大的进展,但阻塞性黄疸对肝细胞能量方面的影响尚不是十分明确。笔者就此做一综述。 | 武飞 关养时 | 2008 | 中国普通外科杂志2008，17，5： | 5 |
| 4 | Effects of hemoglobin concentration on hyperdynamic circulation associated with portal hypertension显示文摘BACKGROUND: Chronic anemia caused by different factors is a common complication in patients with portal hypertension, but attention has been rarely paid to its detrimental effect on hemodynamic status. This study was undertaken to investigate the effects of hemoglobin concentration on hyperdynamic disturbance associated with portal hypertension (PHT). METHODS: According to blood hemoglobin level of 120 g/L, 55 patients with portal hypertension were divided into two groups, anemic and nonanemic. Hemodynamic and clinical data of the patients were analyzed retrospectively. The data were analyzed separately according to the Child classification in an attempt to avoid the effects of differences on hepatic function. RESULTS: Compared with the nonanemic group, the anemic group had an increased cardiac output (7. 4 ± 1. 7 L/ min vs. 6.3+1.9 L/min, P =0. 028), free portal pressure (29. 1 ±3. 1 mmHg vs. 26.8 ±3.3 mmHg, P =0.012), a decreased mean arterial pressure (84.0 ± 10.7 mmHg vs. 97.1 ±12.0 mmHg, P<0.01), and systemic vascular resistance (866 ±215 dyn/s ·cm5 vs. 1207 ±317 dyn/s ·cm5, P <0.01). Similar results were obtained when Child A and Child B-C patients were analyzed separately. Multivariate logistic regression revealed that the concentrations of hemoglobin (standard coefficient =0.31, P=0.01) and albumin (standard coefficient =0.21, P=0.04) were independent factors influencing the systemic vascular resistance in PHT patients. CONCLUSIONS: Anemia aggravates the hyperdynamic circulation of portal hypertension. Hemoglobin concentration is an important variable for evaluating the degree of hemodynamic disturbance in PHT patients. | Rong Hua, Hui Cao and Zhi-Yong Wu Department of General Surgery, Renji Hospital, Shanghai 200127, China | 2006 | Hepatobiliary & Pancreatic Diseases International2006，5，2： | 3 |
| 5 | 食管静脉曲张发病机制研究进展显示文摘食管静脉曲张是门脉高压症的严重并发症之一,可引起致死性大出血。因此成为门脉高压症的研究重点,近些年来不少学者致力于食管解剖结构改变和分子机制方面的研究并且取得了很大的进展。本文将对此进行概述。 | 范铁艳 程留芳 | 2007 | 辽宁医学院学报2007，28，6： | 1 |
| 6 | 阻塞性黄疸时内毒素与Toll样受体显示文摘 | 谢毅 姜雨刚 林木生 | 2006 | 广东医学院学报2006，24，6： | 1 |
| 7 | 内皮素-1在脂多糖致大鼠门脉高压症中作用的体外研究显示文摘目的:研究内皮素-1(ET-1)在脂多糖致门脉高压中的作用及其机制。方法:分离、纯化大鼠星状细胞,培养在胶原凝胶上,应用ET-1-ASON和LPS序贯共培养(实验组),以正义、错义ASON作为对照,检测凝胶收缩情况;应用放射免疫法检查培养上清液的ET-1浓度;免疫印迹法检测各组细胞α-actin表达情况;RT-PCR检测各组细胞ET-1表达情况。结果:实验组的孔胶原直径缩小至93.3%±3.8%,胶原直径较对照组大(P<0.05);实验组HSC培养基上清液ET-1为(49.8±7.4)ng/L,显著低于对照组(P<0.01);实验组HSC表达β-ac-tin较对照组弱;实验组HSC表达ET-1 mRNA显著低于对照组(P<0.01)。结论:ET-1在脂多糖致门脉高压中通过抑制星状细胞活化而起重要作用,ET-1-ASON在控制脂多糖致门脉高压中具有应用前景。 | 毕向军 陈旻湖 陈文红 陈为 王锦辉 朱森林 | 2007 | 中国病理生理杂志2007，23，3： | 1 |
| 8 | 梗阻性黄疸梗阻解除后黄疸加重的原因分析显示文摘目的分析我院53例梗阻性黄疸患者经手术解除梗阻后黄疸加重原因,探讨该类患者诊治方法。方法回顾性分析2008年1月~2016年6月本院53例胆道梗阻患者术后非手术创伤性所致黄疸的病例资料。结果术后胆汁多次培养为大肠埃希菌和革兰阴性菌感染6例;53例术前总胆红素36~319μmol/L(参考范围15~25μmol/L),结合胆红素34~203μmol/L,术前黄疸平均时间4周;术中操作欠妥3例;手术时间在4h以上者15例;术中失血过量,血压低、缺氧及休克21例;输注库存血3例;5例术中胆道镜注水压超过470mm H 2 O;53例均于术后第1~2天发现黄疸血清总胆红素70~332μmol/L。术后黄疸高峰持续时间平均为3周,最短为术后2周,最长达术后半年之久。最早出现黄疸消退的病例为9天。53例患者均予保守后痊愈出院,无因黄疸引起的房性早博、肾功能障碍、出血倾向及急性胃病变等并发症,随访1年正常。结论胆道术后黄疸是较常见的并发症,非手术创伤性黄疸是其中之一,有多种因素,需仔细查找原因,通过非手术方法治疗,避免过度剖腹手术探查。 | 江志沅 王三贵 邓莫根 王海峰 | 2017 | 中国医药科学2017，7，22： | 0 |
| 9 | 内皮素反义基因治疗门静脉高压症的研究显示文摘目的研究内皮素-1反义寡核苷酸(ET1-ASON)在内毒素(LPS)致门静脉高压中的作用。方法应用 ET1-ASON 预处理后将 LPS 以1 mg/kg 体重腹腔注射大鼠,以正义、错义 ET1-ASON 和生理盐水作为对照,4 h 后检测大鼠 PVF、PVP、PVR 和 IVCP应用放射免疫法、RT-PCR 检测各组门静脉血和肝脏的 ET1表达情况。结果 ET1-ASON 处理组大鼠门静脉血浆和肝脏组织ET1表达减低;PVR 和 PVP 较对照组明显降低,PVF 无明显改变。结论 ET1-ASON 在内毒素致门脉高压中主要通过降低 PVR 起作用。 | 毕向军 陈旻湖 陈文红 陈为 王锦辉 朱森林 | 2006 | 中华肝胆外科杂志2006，12，4： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员