血清总胆汁酸与胆碱酯酶联合检测在肝病中的应用

目的：探讨血清总胆汁酸（TBA）和胆碱酯酶（CHE）水平与肝病诊断的关系。方法：对200例肝病患者分别检测血清TBA和CHE浓度。结果：血清TBA在各肝病组明显升高,与肝炎病程呈正相关;血清CHE在各肝病组明显降低,与肝病病程呈负相关。结论：联合检测血清TBA和CHE有助于发现肝脏合成和代谢功能的早期实质性损害。     

强化胰岛素治疗对脓毒症患者血清血管性假血友病因子、内皮素1和一氧化氮浓度及预后的影响

目的：探讨强化胰岛素治疗（IIT）对脓毒症患者血清血管性假血友病因子（v WF）、内皮素1（ET-1）和一氧化氮（NO）浓度及预后的影响。方法：将90例脓毒症患者随机分为强化胰岛素治疗组（IIT组）和常规胰岛素治疗组（CIT组）。在治疗前、治疗后3 d、7 d用酶联免疫吸附法（ELISA）检测2组患者血清v WF、ET-1和NO的浓度。同时记录2组患者ICU住院时间、机械通气时间、ICU最后1 d的APACHEⅡ评分、28 d病死率及低血糖发生率。结果：IIT组患者血清v WF、ET-1浓度较CIT组均明显降低（P〈0.05）,NO浓度较CIT组均明显升高（P〈0.05）,且IIT组患者ICU住院时间、机械通气时间、ICU最后1 d的APACHEⅡ评分、28 d病死率较CIT组均明显降低（P〈0.05）,但两组患者低血糖发生率相近（P〉0.05）。结论：IIT可以使脓毒症患者血清v WF、ET-1浓度降低及NO浓度升高,同时可以降低患者病死率,改善预后。     

Chemerin及NO在子痫前期患者血清中的相关性分析

目的：通过检测Chemerin及NO在子痫前期患者血清中的浓度,分析Chemerin与NO的相关性,探讨Chemerin在子痫前期患者发病过程中作用,为子痫前期患者早期诊断提供新思路。方法：用Elisa法检测血清中Chemerin的浓度,用硝酸还原法检测血清中NO的浓度,其中实验组为子痫前期患者30例,对照组为正常妊娠孕妇20例。结果：Chemerin在重度子痫前期患者血清中的浓度为（70.12±3.12）pg/mL,轻度子痫前期血清中的浓度为（68.84±4.24）pg/mL,正常孕妇血清中的浓度为（63.72±6.66）pg/mL,样本经t检验,具有统计学意义（P〈0.05）,即Chemerin在人血清中的浓度：重度子痫前期患者〉轻度子痫患者〉正常孕妇,并且随着病情越重其浓度越高。NO在血清中浓度经t检验具有统计学意义（P〈0.05）,随着病情进展其浓度越低,即重度子痫患者〈轻度子痫患者〈正常孕妇;血清中Chemerin及NO的浓度呈负相关（r=-0.524,P〈0.05）。结论：Chemerin与NO呈负相关,Chemerin可能引起的IR,IR状态下NO合成减少,引起全身血管内皮细胞受损;Chemerin亦能引起炎症反应,引起体内内皮细胞合成NO减少,参与子痫前期的发生、发展。     

类风湿关节炎患者血清、关节液一氧化氮及肿瘤坏死因子－α的检测及意义

为探讨一氧化氮（NO）和肿瘤坏死因子－α（TNF－α）在类风湿关节炎（RA）中的作用,检测了50例RA患者的关节液及血清中NO浓度和血清中TNF－α浓度,与30名健康人血清中NO浓度进行比较,结果表明,RA组血清中NO浓度（0．46&;#177;0．07μmol/L）高于正常对照的2倍,差异有非常显著意义（P＜0．01）,而且关节液中NO浓度（0．95&;#177;0．17μmol/L）也显著高于血清中浓度（P＜0．01）。RA组血清中TNF－α（65．12&;#177;2．46μg/L）与正常对照相比差异有显著意义（P＜0．01）,而且RA组血清中NO浓度与TNF－α成正相关（r=0.16,P&;lt;0.05)。结论：TNF－α和NO在RA的发病中起到一定作用。TNF－α在体内可以使巨噬细胞产生大量的NO,关节液中增加的NO随关节液循环进入血液中,造成身体其他部位的损伤。     

超敏C-反应蛋白在肝病诊断中的应用价值

目的：研究在不同肝病患者血清中超敏C-反应蛋白（hs-CRP）在肝病诊断中的应用价值。方法：选择肝癌患者40例、肝硬化患者48例、肝炎患者68例（急性肝炎42例、慢性肝炎26例）作为肝病患者组（排除同时引起hs-CRP水平升高的其他疾病）;收集肝肾功能、血脂、血糖、白细胞、心电图等体检指标正常的体检人员140例作为对照组,进行血清超敏C-反应蛋白测定。结果：各组肝病患者血清中超敏C-反应蛋白与对照组相比明显升高,差异有统计学意义（P〈0.01）,组间比较差异有统计学意义（P〈0.01）。结论：肝病患者血清中hs-CRP水平明显升高,各组病情不同变化也不同。检测hs-CRP对肝病的辅助诊断、疗效观察及预后判断有重要价值。     

血清高密度脂蛋白胆固醇水平用于评价肝脏合成功能的价值

目的：探讨血清高密度脂蛋白胆固醇（HDL-C）水平用于评价肝脏合成功能的价值。方法选择我院收治的肝病患者及体检正常者作为研究对象并进行分组,应用全自动生化分析仪对研究对象的血清HDL-C水平进行测定,并进行组间结果比较。结果对照组HDL-C水平为（1.28±0.20）mmol/L,肝病组为（0.77±0.15）mmol/L,其中肝炎组为（0.81±0.13）mmol/L,肝硬化组为（0.68±0.14）mmol/L,肝癌组为（0.54±0.05）mmol/L。肝病组以及肝病组内肝炎、肝硬化、肝癌患者的血清HDL-C水平均显著低于对照组（P＜0.05）;肝病组内肝硬化、肝癌患者的血清HDL-C平均值均显著低于肝炎患者（P＜0.05）;肝癌患者血清HDL-C平均值显著低于肝硬化患者（P＜0.05）。结论血清HDL-C的具体水平可以反映肝病患者的肝脏合成功能,其数据水平越低,表示损伤越严重,查明其具体水平,对于及时进行治疗具有极大的参考价值。     

妊娠期高血压疾病患者血浆总同型半胱氨酸浓度监测

目的：探讨妊娠期高血压疾病患者血浆总同型半胱氨酸（tHcy）浓度检测的临床意义。方法：采用荧光偏振免疫分析法检测300例妊娠期高血压疾病患者（其中轻度231例,重度69例）和300例正常同期妊娠妇女血浆tHcy浓度,同步取静脉血采用离子捕捉免疫分析法检测其血清叶酸和微粒子酶联免疫分析法检测其血清维生素B12的浓度。结果：血浆tHcy浓度妊娠期高血压疾病患者[（11.79±3.52）μmol·L^-1]显著高于正常妊娠组[（6.72±2.43）μmol·L^-1]（P〈0.01）,且重度患者[（16.85±5.61）μmol·L^-1]显著高于轻度患者[（11.46±3.22）μmol·L^-1]（P〈0.01）;血清叶酸浓度妊娠期高血压疾病患者[（11.74±3.58）nmol·L^-1]显著低于正常妊娠组[（14.91±4.63）nmol·L^-1]（P〈0.01）,血清维生素B12浓度妊娠期高血压疾病患者[（328.89±90.06）pmol·L^-1]显著低于正常妊娠组[（405.37±94.18）pmol·L^-1]（P〈0.01）。结论：妊娠期高血压疾病患者血浆tHcy浓度显著上升,血清叶酸、VitB12浓度显著下降。随着病情的加重,妊娠期高血压疾病患者血浆tHcy浓度呈逐渐上升趋势,监测血浆tHcy浓度对了解妊娠期高血压疾病病情具有重要意义。     

急性冠脉综合征患者血清尿酸与血清NO的相关性

目的：探讨急性冠脉综合征急性期血清尿酸水平与一氧化氮（NO）的相关性。方法：对纳入的39例ACS患者按血清尿酸浓度高低分为A、B、C3组,以健康人群体检共31例为正常对照组,检测血清NO的变化。结果：尿酸值越高NO值越低,尿酸大于421μmol/L时更为显著,P〈0.001。结论：血清尿酸升高与ACS的发生发展和预后密切相关。     

盐敏感性高血压患者血清非对称二甲基精氨酸的测定及其意义

目的：探讨盐敏感性高血压患者血清非对称二甲基精氨酸（asymmetric dimethylarginine,ADMA）的测定及其意义。方法：选取100例盐敏感性高血压患者为观察组,选取100例健康体检者为对照组。比较两组血清ADMA水平、血清一氧化氮（nitric oxide, NO）水平;观察不同分级的盐敏感性高血压患者血清ADMA水平差异;采用Pearson相关分析分析血清ADMA水平与血清三酰甘油（triglyceride, TG）、血清总胆固醇（total cholesterol, TC）、血清低密度脂蛋白胆固醇（low density lipoprotein cholesterol , LDL-C）、血清高密度脂蛋白胆固醇（high density lipoprotein cholesterol, HDL-C）、收缩压（systolic blood pressure,SBP）、舒张压（diastolic blood pressure,DBP）的相关性。结果：观察组血清ADMA和NO水平分别为（3.8±0.8）μmol/L、（33.1±8.9）μmol/L;对照组血清ADMA和NO水平分别为（2.3±0.7）μmol/L、（54.4±10.2）μmol/L,两组比较差异具有统计学意义（P<0.05）。随着高血压分级的增高,患者血清ADMA水平明显增加,血清NO水平明显降低,I级、II级、III级患者间血清ADMA及NO水平比较差异显著（P<0.05）。 Pearson相关分析结果显示,观察组患者血清ADMA水平与SBP、DBP、LDL-C、HDL-C、TC、TG呈现正相关（P<0.05）。结论：血清ADMA水平与盐敏感性高血压的发生发展密切相关,对于病情判定和治疗具有一定价值。     

不同病原体中枢神经系统感染患者血清和脑脊液中一氧化氮 总一氧化氮合酶的动态变化

目的观察不同病原体所致中枢神经系统（CNS）感染患者脑脊液（CSF）及血清中一氧化氮（NO）浓度、总一氧化氮合酶（NOS）活力的动态变化，为临床鉴别不同病原体所致中枢神经系统感染提供实验室依据。方法硝酸还原酶法和化学比色法检测30例中枢神经系统感染患者治疗前、治疗2周后CSF中及入院时、住院第3、5、9、14天血清中NO浓度、总NOS活力的动态变化。结果中枢神经系统感染患者不同病原体所致病毒性脑膜炎、化脓性脑膜炎、结核性脑膜炎组不同时点血清NO浓度、总NOS活力组间比较，差异均无统计学意义（P〉0.05）；病毒性脑膜炎、化脓性脑膜炎、结核性脑膜炎患者治疗前、治疗2周后脑脊液中NO浓度、总NOS活力之间差异均无统计学意义（P〉0．05）。结论血清中NO浓度、总NOS活力尚不能作为化脓性脑膜炎、病毒性脑膜炎、结核性脑膜炎临床鉴别诊断的实验室依据之一。     

Serum nitric oxide metabolite (NO(x)) levels in hypertensive patients at rest: a comparison of age, gender, blood pressure and complications using normotensive controls

1. Hypertensive patients have pathophysiological changes such as atherosclerosis, endothelial dysfunction and inflammations. The patients' serum nitric oxide metabolite (nitrate/nitrite; NO(x)) levels were measured in peripheral blood using normotensive controls for comparison. 2. The NO(x) levels in 175 hypertensive patients with or without comorbid diseases (aged 37-95 years; average 50.6 +/- 0.8 years) were compared with those in 80 normotensive controls (aged 25-73 years; average 37.1 +/- 1.8 years). 3. The NO(x) levels increased with age in both the normotensive and hypertensive women, but not in men. No difference was noted in the NO(x) levels between the normotensive and hypertensive patients without comorbid diseases. The mean value of NO(x) in male hypertensive patients aged under 50 years was close to that of female patients aged 51-60 years. Hypertensive males aged 61-70 years showed almost the same NO(x) levels as those of female patients aged over 81 years. A male group of hypertensive patients with diabetes, hyperlipaemia and renal disorder had a significantly higher NO(x) level compared with a normotensive control group. However, in female groups, only hypertensive patients with hyperlipaemia showed higher serum NO(x) values compared with the normotensive group. 4. These findings suggest that: (i) the occurrence of NO(x) in the serum is not solely the outcome of high blood pressure; (ii) higher serum NO(x) levels in older women are because of an oestrogen deficiency-induced cardiovascular disease; (iii) ageing effects on the circulation system are more apparent in men than in women; and (iv) measurement of NO(x) levels in the serum is helpful for understanding the pathological progress in male hypertensive patients with diseases such as diabetes mellitus, hyperlipaemia and renal disorder.     

Study of interaction between nitric oxide and ACE activity in STZ-induced diabetic rats: role of insulin.

The precise mechanisms of vascular diseases in patients with insulin-dependent diabetes mellitus (IDDM) are not clearly understood. There are evidences of alteration in mechanisms involved in regulating vascular tone including increased ACE activity and decreased NO production in STZ diabetic rats. Insulin treatment may reverse these changes by an unknown mechanism. This study sought to examine the interaction of ACE activity and NO and how insulin treatment affected these mechanisms. Four groups of eight male Sprauge-Dawely rats including control (C) and three diabetic groups (D, IT and LIT) were used in this study. Diabetes induced by injection of 60 mg kg(-1) STZ i.p. After induction of diabetes IT group treated with insulin (10 units kg(-1) daily s.c.) for 4 weeks. LIT group received the same amount of insulin and N(omega)-nitro-l-arginine methyl ester (L-NAME; 20 mg kg(-1) i.p.) for the same period. The D group was diabetic control that treated with saline. ACE activity was determined by HPLC method. At the end of study in D group ACE activity was increased in aorta, heart, lung and serum but Serum NO(x) (nitrate and nitrite) concentration decreased compared to C group. These values were reversed to normal by insulin treatment in IT group. In LIT group the ACE activity remained elevated only in aorta and heart while the serum NO(x) was lower than control group. It is concluded that ACE reducing activity of insulin in aorta and heart of STZ-induced diabetic rats may be mediated by elevation of NO by insulin treatment.     

HCV肝炎婴儿血清一氧化氮和免疫球蛋白水平变化的临床意义

目的：探讨HCV肝炎婴儿血清一氧化氮（nitric oxide。NO）和免疫球蛋白（immunoglobulin，垴在肝脏损伤发病过程中的临床意义。方法：IgO、IgA、IgM采用速率散射比浊法，NO采用终点法。结果：与对照组相比，急性期患儿血清中NO水平显著升高，IgG、ISA含量显著降低。恢复期和急性期相比，患儿血清中NO含量有所下降但仍高于对照组，IgG、IgM、IgA均有所升高，但除IgM外均较对照组低。在疾病变化过程中IgG、IgM、IgA的下降与NO的升高成负相关（P〈0．05）.结论：NO与婴儿肝炎综合征的严重程度有关且在一定程度上能调节体液免疫。     

ENDOGENOUS NITRIC OXIDE PRODUCTION IS AUGMENTED AS THE SEVERITY ADVANCES IN PATIENTS WITH LIVER CIRRHOSIS

• 1 Since endothelium-derived nitric oxide (NO) is a potent vasodilator and degraded into nitrous ions, we measured the serum nitrate ion (NO₃^?) and the amount of urinary excretions of NO₃^? as an index for endogenous NO to ascertain whether NO formation is augmented in patients with chronic liver diseases.
• 2 Using inpatients suffering from chronic liver diseases, serum levels and urinary excretions of NO₃^? were measured by using high-performance liquid chromatography with an anion exchange column.
• 3 Among the four patient groups of normal controls, and those with chronic liver diseases such as chronic active hepatitis, compensated cirrhosis, and decompensated cirrhosis the serum level of NO₃^? showed the highest level in a patient group with decompensated cirrhosis. The amount of urinary excretion of NO₃^? was significantly increased in both groups of patients with liver cirrhosis compared with the control group and patients with chronic active hepatitis. Patients with chronic active hepatitis did not show any difference between the normal control group. The amount of urinary excretion of NO₃^? correlated significantly and negatively with the level of serum albumin (P<0.05) and counts of platelets (P< 0.01) in patients with compensated cirrhosis.
• 4 These findings suggest that the production of endogenous NO is augmented in patients with liver cirrhosis, particularly in a decompensated subgroup. Increases in the production of endogenous NO correspond to the progress of liver cirrhosis, but not in patients with chronic hepatitis.

     

Mushroom insoluble polysaccharides prevent carbon tetrachloride-induced hepatotoxicity in rat

The aim of the present study was to investigate the effect of mushroom insoluble non-starch polysaccharides (MINSP) on the carbon tetrachloride (CCl₄)-induced hepatic damage in rat. MINSP (100 and 200 mg/kg) administered daily orally for 15 days before CCl₄ (1.5 ml/kg). The effect of MINSP treatment was also examined in normal rats. Normal groups treated with MINSP showed significant decrease in serum activities of the liver enzymes, lipid peroxides and nitric oxide (NO) in the liver. Reduced glutathione (GSH) and total proteins (TP) contents in liver homogenate also increased after treatment with only MINSP for 15 days. In CCl₄-treated rats, significant elevation in serum liver enzymes, increased lipid peroxides and NO in the liver, and depletion of hepatic-GSH level were observed. Pre-treatment with MINSP significantly ameliorated the tested parameters when compared with CCl₄-treated group. It improved the antioxidant activity of the liver in a dose-dependent manner. Histopathological examination of hepatic tissue revealed that MINSP administration alone protected hepatocytes from the damage induced by CCl₄. Conclusion: MINSP are safe; it could be used as fat replacer in processing low fat diet. MINSP represents a good functional food and liver supporter for patient suffering from various liver diseases.     

白藜芦醇影响一氧化氮途径对大鼠急性酒精性肝损伤的保护作用

目的研究白藜芦醇（resveratrol,Res）对酒精性肝损伤后肝组织氧化反应和炎性反应的影响及与一氧化氮（NO）、诱导型一氧化氮合成酶（iNOS）通路的关系。方法大鼠灌胃给予55度红星二锅头复制肝损伤模型。大鼠随机分为正常对照组、肝损伤模型对照组、Res低剂量组（25 mg.kg-1）、Res中剂量组（50 mg.kg-1）、Res高剂量组（100 mg.kg-1）,每日2次,连续7 d。采用试剂盒测定肝脏组织乳酸脱氢酶（LDH）、活性氧（ROS）、还原型谷胱甘肽（GSH）、NO、iNOS和血清IL-10、IFN-γ水平。Western blot测定iNOS表达,RT-PCR测定iNOS mRNA表达。结果与正常对照组相比,酒精性肝损伤模型组肝组织LDH、ROS、NO浓度显著升高（P〈0.01）、GSH显著下降（P〈0.01）,血清IFN-γ水平显著升高、IL-10显著降低（P〈0.01）,肝组织iNOS和iNOS mRNA表达增加（P〈0.01）。与模型组相比,Res显著降低肝脏组织ROS、LDH、NO浓度（P〈0.01）,降低血清IFN-γ水平和升高血清IL-10与肝脏组织GSH含量（P〈0.01）,减少iNOS和iNOS mRNA表达（P〈0.01）。结论 Res可能通过NO通路,消除氧化性应激状态,改变炎性因子水平,对酒精性肝损伤发挥防治作用。     

泊洛沙姆407诱发金黄地鼠脂质代谢紊乱模型及其初步机制

采用泊洛沙姆(poloxamer 407,P-407)诱导金黄地鼠形成脂质代谢紊乱实验动物模型,并对其脂质代谢紊乱机制进行初步探讨;同时评价该模型对两类市售调脂药物的反应性。选择6周龄的雄性金黄地鼠腹腔注射P-407,首剂量为300 mg·kg-1,之后每72 h以200 mg·kg-1的维持剂量腹腔注射。与正常对照组相比,模型组血清中TG、TC、free-CHO、CE、FFA及apoB的水平均显著升高,LDL-C也有明显升高趋势;另外,模型组血清MDA和NO的含量显著增加。考察肝脏中脂质转运相关酶基因的转录水平变化,发现该模型肝脏中LCAT及SR-BⅠ的mRNA表达水平降低,HMG-CoA还原酶mRNA表达水平显著增加,以上3种酶的基因表达差异可能参与导致了该模型血脂代谢紊乱。在该脂质代谢紊乱模型中,分别给予非诺贝特(100 mg·kg-1)和阿托伐他汀(50 mg·kg-1),每日灌胃1次,连续2周,两种药物均可显著改善其血清脂质代谢紊乱和机体氧化应激及炎症状态。研究提示,雄性金黄地鼠通过连续多次腹腔注射P-407可形成持续性高血脂症,方法简便、形成时间短,且对药物的反应性良好。     

肠安颗粒治疗肠易激综合征的药效学研究

目的进行肠安颗粒治疗肠易激综合征(IBS)的药效学研究。方法大鼠60只随机分为空白对照组,模型对照组,匹维溴铵组,肠安颗粒高剂量组(生药28.4g·kg~(-1))、中剂量组(生药14.2 g·kg~(-1))、低剂量组(生药7.1 g·kg~(-1)),采用荧光分七光度法测定血清中5-羟色胺(5-HT)的含量,硝酸还原酶法测定血清中-氧化氮(NO)含量,考察动物体重、血清中5-HT含量变化、血清中NO含量变化,并观察结肠组织的病变情况。结果肠安颗粒高、中、低剂量组对模型大鼠体重下降有明显的改善,与模型对照组比较差异显著(P<0.01),与匹维溴铵组作用相当;肠安颗粒高、中、低剂量均可明显提高血清中5-HT和NO含量;组织学检查结果表明,肠安颗粒高、中剂量可明显改善动物结肠的炎症症状,与模型对照组比较差异显著,与匹维溴铵组无明显差异。结论肠安颗粒可改善IBS大鼠体重与结肠炎症,其原因可能与提高血清中5-HT和NO含量有关。     

血管调节因子在脑缺血中的作用及其相互关系

目的：探讨在缺血性脑血管病的发生发展中，相关的血管调节因子的作用及相互关系。方法：采用线栓法制作大鼠局灶性脑缺血模型后，分别给予一氧化氮合酶(NOS)抑制剂L—NAME(B组)及内皮素(ET)受体拮抗剂PD142893(C组)，在术后3，6，24h进行神经病学评分，术后24h测定血浆ET及NO含量，计数梗死边缘区及海马CA1亚区存活神经元数目。结果：与单纯缺血组(A组)相比较，C组神经功能损害减轻，梗死边缘区及海马CA1亚区存活神经元数增多，而B组的改变则相反。同时，B组血浆ET含量升高，而C组血浆NO含量降低。结论：ET受体拮抗剂对缺血脑组织有保护作用。NO在脑缺血急性期有神经保护作用。脑缺血后NO抑制了ET的产生和释放，而ET则促进了NO的产生。     

Effect of the nitric oxide donor and the nitric oxide synthase inhibitor on the liver of rats with chronic hepatitis induced by dimethylnitrosamine

The present study was designed to examine the effects of the donor of nitric oxide (NO), NaNO(2) and the inhibitor of NO synthase, N(omega)-nitro-L-arginine (L-NNA), on the development of dimethylnitrosamine (DMNA)-induced chronic hepatitis in rats. L-NNA decreased rat survival and enhanced the severity of hepatic encephalopathy in the DMNA-treated animals. The aggravation of the morphological signs of hepatitis, the activation of serum alanine aminotransferase and cytosolic superoxide dismutase activities and the increase in the liver malondialdehyde content were observed in this group. The treatment with NaNO(2) improved liver morphology, decreased serum marker enzyme activities, lowered the activities of alpha-D-mannosidase and N-acetyl-beta-D-glucosaminidase compared to the DMNA-treated group. The results of the morphological and biochemical studies suggest that L-NNA increased DMNA-induced liver damage, whereas NaNO(2) partially prevented the development of chronic hepatitis. It is proposed that the opposite effects of L-NNA and NaNO(2) are partially explained by a modulation of the free radical-dependent processes in the liver.