Changes in serum ammonia concentration in cirrhotic patients with Helicobacter pylori infection

Objective To study whether liver cirrhosis associated with Helicobacter pylori (H. pylori) infection will induce increased serum ammonia and whether the peripher al serum ammonia reflects the level of portal vein serum ammonia. Methods Blood was taken from the portal vein and the cubital vein in cirrhotic patients with and without H. pylori infection and non-cirrhotic patients (splenic rupture) with and without H. pylori infection, and the serum ammonia was measured.Results The mean levels of serum ammonia in the group of cirrhotic patients with H. pylori infection were 167.82±8.97 μmol/L (portal vein) and 142.2±13.35 μmol/L (cubital vein). They were increased significantly as compared with cirrhotic patients without H. pylori infection (47.68±12.03 μmol/L portal vein and 37.23±7.04 μmol/L cubital vein), and also compared with the groups of splenic rupture patients with and without H. pylori infection ( P <0.01). There was no significant difference between the serum ammonia level of the cubital vein and portal vein (P>0.05).Conclusions H. pylori infection can induce an increase in serum ammonia in patients with liver dysfunction, and the peripheral serum ammonia measurement may replace the portal vein serum ammonia as a monitoring method. Eradication of H. pylori in cirrhotic patients may prevent hepatic encephalopathy (HE).     

Effects of catecholamine-β-adrenoceptor-cAMP system on severe patients with heart failure

Objective To investigate the association between catecholamine-β-adrenoceptor (β-AR)-adenosine 3’, 5’-monophosphate (cAMP) system and long-term　prognosis in patients with chronic heart failure (CHF).Methods The study population comprised 73 patients with CHF (EF: 23%±10%) with a mean follow-up of 3.8±1.9 years. Plasma levels of norepinephrine (NE) were measured using high performance lipid chromatography, β-adrenergic receptor density (Bmax) and the content of cAMP in peripheral lymphocytes were calculated using 3H-dihydroalpneolo as ligand and competitive immunoassay, respectively. Deaths due to cardiovascular events within the follow-up period were registered.Results The total mortality was 64.7%, 57.4% of which was for cardiogenic (worsening heart failure: 32.4%; sudden death: 25.0%). In the cardiogenic death group, plasma levels of NE and epinephrine (E) (3.74 nmol/L±0.09 nmol/L and 3.17 nmol/L±1.0nmol/L) and the contents of peripheral lymphocyte cAMP (3.64 pmol/mg protein±1.4 pmol/mg protein) were significantly increased as compared with the survival group (2.68 nmol/L±0.07 nmol/L, 2.41 nmol/L±0.24 nmol/L and 2.73 pmol/mg protein±0.9 pmol/mg protein, respectively, all P<0.01). In the sudden death group, plasma levels of NE and E (5.01 nmol/L±0.06 nmol/L and 4.13 nmol/L±0.08 nmol/L) were significantly increased as compared with the worsening heart failure group (2.49 nmol/L±0.07 nmol/L and 2.33 nmol/L±0.8 nmol/L, all P<0.001) and to the survival group (2.68 nmol/L±0.07 nmol/L and 2.41 nmol/L±0.14 nmol/L, all P<0.01). The incidences of sudden death were 0%, 75%, and 100% (χ2=16.018, P<0.01) in patients with plasma NE<2.5 nmol/L, NE 2.5 nmol/L-4.5 nmol/L, and NE>4.5 nmol/L, respectively. In the worsening heart failure group, the content of peripheral lymphocyte cAMP (4.46 pmol/mg protein±0.18 pmol/mg protein) was significantly increased compared with the sudden death group (2.39 pmol/mg protein±0.9 pmol/mg protein, P<0.001) and to the survival group (2.73 pmol/mg protein±1.1 pmol/mg protein, P<0.001). The worsening heart failure death occurences were 5.0%, 72.2%, and 100% (χ2=14.26, P<0.01) in patients with a content of peripheral lymphocyte cAMP <2.5 nmol/L, cAMP 2.5 nmol/L-4.5 nmol/L, and cAMP>4.5nmol/L, respectively. Bmax in peripheral lymphocyte was not significantly different (P>0.05) among the sudden death, worsening heart failure, and survival groups in CHF patients.Conclusions Plasma levels of catecholamine increase significantly, and Bmax and the contents of cAMP in peripheral lymphocytes decrease significantly in patients with CHF. High plasma catecholamine levels may be associated with sudden death, and high intralymphocyte cAMP content may be associated with worsening heart failure in CHF patients.     

An animal study of portal hypertension

For the purpose of elucidation the mechanism of portal venous resistance and portal venous blood flow in maintaining an elevated portal hypertension. The splanchnic and systemic hemodynamics were evaluated in portal hypertensive rat model, which is induced by partial portal vein ligation (PVL). Organ blood flow and portal-systemic shunting were measured by radio-active microsphere techniques. In this study all the PVL rats had higher mean portal venous pressure (15.2 +/- 1.6 mmHg) when compared to the Sham-operation control rats (5.3 +/- 1.2 mmHg). Furthermore, portal systemic shunting was significantly higher in the 14th day PVL rats (87.2 +/- 3.6%) than control rats (0.3 +/- 0.1%) (p less than 0.05). There was a rapid increase in portal venous inflow from the 4th day (6.1 +/- 0.8 vs 4.2 +/- 0.7 ml/min/100 gm BW, p less than 0.05) in the PVL rats than in control rats. However, the total peripheral resistance and splanchnic arterial resistance were reduced in the 14th PVL rats than control rats. The Cardiac index was much higher in the 14th PVL rats than control rats. Thus our results demonstrate that portal hypertension is maintained by a hyperdynamic portal venous inflow. This model is reproducible for us to study portal hypertension within a short period of time.     

血小板活性因子及其拮抗剂对大鼠肝硬化门脉高压的影响

目的探讨肝硬化时肝脏和血循环中血小板活性因子(PAF)的变化以及其对门脉高压的影响。方法CCl4腹腔注射8周(0·15ml/kg,2次/周)诱导大鼠肝硬化,快速3H-PAF液闪检测肝及循环中PAF水平;受体饱和结合实验分析肝组织PAF结合能力;监测外源性PAF及其拮抗剂BN52021对门脉压和系统动脉压的影响。结果与对照组相比,肝硬化时肝内PAF、肝脏输出PAF及肝内生PAF水平明显升高,分别4·0ng/g±0·4ng/gvs2·7ng/g±0·5ng/g(P<0·01)、6·3ng/ml±0·6ng/mlvs3·4ng/ml±0·6ng/ml(P<0·01)、1·0ng/ml±0·6ng/mlvs-0·3ng/ml±0·5ng/ml(P<0·01);肝组织PAF结合能力Bmax明显升高(2·8±0·21)fmol/μg膜蛋白vs(0·9±0·06)fmol/μg膜蛋白,P<0·01,而受体亲和力Kd差异无统计学意义(8·0nmol/L±1·3nmol/Lvs5·8nmol/L±1·0nmol/L,P>0·05)。肝硬化组基础门脉压升高(12·2mmHg±0·7mmHgvs5·3mmHg±0·6mmHg,P<0·01),系统动脉压降低(82mmHg±10mmHgvs114mmHg±9mmHg,P<0·01)。门脉注入PAF(1μg/kg)后,肝硬化组门脉压提高了32%(12·1mmHg±0·6mmHgvs16·0mmHg±0·7mmHg,P<0·01),升高幅度约为对照组的227%(4·1mmHg±1·0mmHgvs1·8mmHg±0·3mmHg,P<0·01),而系统动脉压在两组均下降(肝硬化组由82mmHg±10mmHg降至48mmHg±4mmHg,P<0·01;对照组由114mmHg±9mmHg降至52mmHg±4mmHg,P<0·01)。门脉注入BN52021(5mg/kg),肝硬化组门脉压降低了16%(14·6mmHg±1·6mmHgvs12·3mmHg±0·8mmHg,P<0·05),而系统动脉压在肝硬化组和对照组均无明显变化(P>0·05)。结论肝硬化时肝脏合成PAF明显增加是循环血PAF升高的重要来源,并上调节肝的血流动力学影响门脉高压形成,其作用可被其拮抗剂BN52021部分逆转。     

游离脂肪酸诱导的胰岛素抵抗对血浆ghrelin水平的影响

目的　探讨正糖 高胰岛素钳夹及游离脂肪酸 (FFA)对大鼠血浆ghrelin浓度的影响。方法　建立清醒状态下大鼠正常血糖 高胰岛素钳夹技术 ,在钳夹前后分别测定大鼠血浆ghrelin浓度 ,脂质灌注组大鼠 12只 ,生理盐水组 12只为对照 ,并用 3 3 H葡萄糖作为示踪剂测定了胰岛素介导的外周和肝糖的代谢。结果　在胰岛素钳夹中 ,脂质灌注组大鼠血浆FFA明显增加 (从 74 2 μmol/L±5 1μmol/L到 2 346 μmol/L± 2 38μmol/L ,P <0 0 1)。脂质灌注组葡萄糖输注率 (GIR)明显低于对照组( 2 0 0 2 4 0min ,平均 12 6mg·kg-1·min-1± 1 5mg·kg-1·min-1vs 34 0mg·kg-1·min-1± 1.6mg·kg-1·min-1,P <0 0 1)。到钳夹结束时 ,下降至相应对照值的 35 % ( 2 4 0min ,12 0mg·kg-1·min-1± 1 9mg·kg-1·min-1vs 34 7mg·kg-1·min-1± 1 7mg·kg-1·min-1,P <0 0 1)。对照组肝糖产率 (HGP)明显被抑制 ( 88% ) ,从 19 0mg·kg-1·min-1± 4 5mg·kg-1·min-1降至 2 3mg·kg-1·min-1± 0 9mg·kg-1·min-1(P <0 0 1)。脂质输注组胰岛素对HGP的抑制作用明显障碍 ( 2 0 0 2 4 0min ,从 18 7mg·kg-1·min-1± 3 0mg·kg-1·min-1到 2 3 2mg·kg-1·min-1± 3 1mg·kg-1·min-1,P <0 0 5 )。钳夹术结束时 ,对照     

分娩方式对新生儿脐血儿茶酚胺水平的影响

目的 比较不同分娩方式对新生儿脐动、静脉血浆儿茶酚胺类激素水平的影响.方法 新生儿共150例,分为正常新生儿组(90名)及胎儿窘迫组(60例).再根据分娩方式的不同分为5组,各30例,分别为阴道分娩组、分娩镇痛组、择期剖宫产组、阴道助产组(施行低位产钳助产术)和急诊剖宫产组.于胎儿娩出断脐后立即采集脐动、静脉血各3 ml,分别置于抗凝管中,即刻离心,分离血浆,采用酶联免疫吸附剂测定(ELISA)法分别测定血浆去甲肾上腺素(NE)、肾上腺素及多巴胺的水平.结果 (1)各组脐动脉血NE及肾上腺素水平差异均有统计学意义(均P＜0.01),其中阴道助产组最高[(73±6) ng/L,(37.8±1.8)ng/L],其次为急诊剖宫产组、阴道分娩组及分娩镇痛组,择期剖宫产组最低[(35±5)ng/L,(27.2±1.2) ng/L].多巴胺水平阴道助产组[(33.7±4.5) ng/L]及急诊剖宫产组[(32.9±4.5) ng/L]高于其他各组,差异均有统计学意义(均P＜0.01);(2)各组脐静脉血NE及肾上腺素水平差异均有统计学意义(均P＜0.01),且高低顺序与脐动脉一致.阴道助产组及急诊剖宫产组多巴胺水平比其他各组高,差异均有统计学意义(均P＜0.01).(3)无论脐动、静脉,胎儿窘迫组NE、肾上腺素、多巴胺水平均高于正常新生儿组,差异有统计学意义(P＜0.01),胎儿窘迫组生后1、5 及10 min Apgar评分均低于正常新生儿组,差异有统计学意义.结论 对于无剖宫产指征的个体,阴道分娩可提高新生儿脐血儿茶酚胺类激素的水平,分娩期自控硬膜外镇痛可抑制新生儿应激反应;与正常新生儿相比,胎儿窘迫者脐血儿茶酚胺水平较高,既是新生儿提高自身对缺氧耐受力的表现,也是其缺氧状态的客观反映.     

环氧化酶2在急性冠脉综合征患者外周血单核细胞中的表达及意义

目的：检测急性冠脉综合征（ACS）患者外周血单核细胞中环氧化酶2（COX-2）mRNA的表达水平并探讨其意义。方法：选择典型急性冠脉综合征患者42例,分离和培养单核细胞,并采用不同浓度的选择性COX-2抑制药（塞来昔布）体外干预。采用RT-PCR法半定量COX-2 mRNA的表达,夹心酶联免疫吸附法（ELISA）测定培养上清液中IL-6和基质金属蛋白酶9(MMP-9)浓度。结果：ACS患者外周血单核细胞中COX-2 mRNA表达（0.61±0.17）较健康对照组（0.11±0.09）明显增强(P<0.05);ACS患者外周血单核细胞培养上清液中IL-6浓度［(97.24±11.21)ng/L］较健康对照组 ［(22.15±6.30)ng/L］显著升高(P<0.05),MMP-9浓度［(41.20±8.41)μg/L］较健康对照组 ［(11.76±4.23)μg/L］显著升高（P<0.05）;ACS患者外周血单核细胞经塞来昔布干预后, 塞来昔布以浓度依赖性方式降低培养上清液中IL-6和MMP-9浓度分别达48%和50%（均P<0.05）。结论：COX-2可能在急性冠脉综合征的炎症反应中起重要作用。     

Alpha-1 adrenergic receptors in liver plasma membranes of cirrhotic patients with portal hypertension: a quantitative study

OBJECTIVE: To investigate the changes of alpha-1 adrenergic receptors in cirrhotic liver and the relationship between the changes and the pathogenesis of portal hypertension. METHODS: The concentration and affinity of alpha-1 adrenergic receptors in the liver plasma membranes of posthepatitic cirrhotic patients with portal hypertension were quantitatively measured using radioligand binding analysis. RESULTS: Compared with 8 controls without hepatic pathological changes, the maximal binding capacity (Bmax) of 9 posthepatitic cirrhotic patients decreased (129.1 +/- 12.0 vs 142.1 +/- 14.1 fmol/mg protein, P > 0.05), dissociation constant (Kd) values increased (0.3945 +/- 0.0974 vs 0.2382 +/- 0.0548 nmol/L, P < 0.01), and the receptor maximal content (RMC) decreased (417.4 +/- 76.8 vs 739.9 +/- 167.6 fmol/g liver, P < 0.01). CONCLUSIONS: The decreased concentration and affinity of alpha-1 adrenergic receptors may play an important role in the metabolic disturbances of catecholamines often seen in some cirrhotic patients, and have implications in the pathogenesis of portal hypertension.     

局部血管紧张素原mRNA的表达与核因子-κB的活化在门静脉高压症性血管病变中的意义

目的探讨肝硬化门静脉高压症(PHT)时局部血管紧张素原mRNA表达与核因子-κB(NF-κB)的活化在门静脉高压症性血管病变中的意义。方法采用逆转录聚合酶链反应(RT-0PCR)方法检测肝硬化门静脉高压症病人脾脏动、静脉组织和正常血管局部血管紧张素原mRNA的表达情况,用化学发光凝胶电泳迁移率实验(EMSA)方法检测局部NF-κB的活性。结果对照组内脾脏动、静脉组织局部血管紧张素原mRNA分别为0.23±0.12、0.18±0.10,显著低于肝硬化门静脉高压症组脾动脉、脾静脉组织局部血管紧张素原mRNA的表达0.48±0.21、0.43±0.16(P<0.05);对照组脾动、静脉局部NF-κB未被检测到明显的活性,而于肝硬化门静脉高压症组检测到显著具有活性的NF-κB表达(P<0.05)。结论肝硬化门静脉高压病人局部血管紧张素原mRNA表达增强,NF-κB的活化,可能是肝硬化门静脉高压症时内脏血管病变形成和发展的原因之一。     

Effect of surgical castration on risk factors for arteriosclerosis of patients with prostate cancer

Objective To analyze the effect of castration on risk factors for arteriosclerosis of patients with prostate cancerMethods Thirty patients with primary regional prostate adenocarcinoma limited to the prostate theca were selected in this study.Serum levels of testosterone (T), free testosterone (FT), dehydroepiandrosterone (DHEA), sex hormone-binding globulin (SHBG), prostatic specific antigen (PSA), triglyceride (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C), low density lipoprotein-cholesterol (LDL-C), apoprotein α(1) (APOα(1)) and apoprotein β (APOβ), insulin, plasma fibrinopeptide A (FPA), plasminogen activator inhibitor-1 (PAI-1) and fibrinogen were determined just prior to, 1 week and 1, 4 and 8 months after castration.Results T, FT and PSA decreased significantly 1 week after castration (21.12±15.11 ng/ml vs 383.9±62.6 ng/ml, P&lt;0.001; 4.08±3.29 pmol/L vs 34.11±11.59 pmol/L, P&lt;0.001; 14.34±7.77 ng/ml vs 23.51±6.57 ng/ml, P=0.001, respectively) and continued to decrease until reaching their lowest levels 8 months after castration.DHEA and SHBG did not undergo any changes.TG, fasting insulin and glucose, 2-hour insulin and glucose levels were significantly elevated 1 month after castration (1.84±0.61 mmol/L vs 1.30±0.40 mmol/L, P&lt;0.05; 18.16±5.57 mU/L vs 9.47±3.81 mU/L, P&lt;0.05; 4.77±0.66 mmol/L vs 3.92±0.34 mmol/L, P&lt;0.05; 65.52±14.78 mU/L vs 36.94±17.12 mU/L, P&lt;0.01; 6.98±0.79 mmol/L vs 6.01±0.23 mmol/L, P=0.001, respectively).TC, LDL-C, FPA and PAI-1 levels were elevated 4 months after castration (6.56±0.99 mmol/L vs 5.29±0.75 mmol/L, P&lt;0.01; 4.09±0.86 mmol/L vs 3.04±0.15 mmol/L, P&lt;0.01; 3.39±1.67 nmol/L vs 1.48±0.50 nmol/L, P&lt;0.01; 27.02±5.98 ng/ml vs 21.78±3.16 ng/ml, P&lt;0.05, respectively), continuing to increase after that point.Insulin sensitive index (ISI) decreased significantly 1 month after surgery (-4.42±0.36 vs -3.50±0.39, P&lt;0.001), and continued to decrease from that point forward.HDL-C, APOα(1), APOβ and fibrinogen remained at pre-operative levels.There was a negative linear correlation between FT and TG, TC, LDL-C, PAI-1, FPA, fasting insulin and glucose, 2-hour insulin and glucose (r=-0.311, -0.384, -0.385, -0.339, -0.353, -0.381, -0.303, -0.460 and -0.395, respectively; P&lt;0.05).A similar phenomenon occurred with T (r=-0.308, -0.309, -0.356, -0.320, -0.430, -0.453, -0.435, -0.483 and -0.512, respectively; P&lt;0.05).T and FT were positively associated with ISI (r=0.555 and 0.501; P&lt;0.001).Conclusions At 8 months follow-up of the study subjects, we found that lower androgen levels have adverse effects on lipid metabolism, coagulative function and insulin sensitivity, related to arteriosclerosis in men.     

急性脑梗死患者血浆尿激酶型纤溶酶原激活物及其受体的表达

目的　检测急性脑梗死患者血浆中尿激酶型纤溶酶原激活物 (uPA)及其受体 (uPAR)的含量变化 ,并探讨其在脑梗死发生发展过程中的作用。方法　应用ELISA双抗体夹心法分别测定89例急性脑梗死患者、30例其他疾病对照组和 30名健康对照组血浆中uPA和uPAR含量 ,并按病情分轻、中、重 3组进行比较。结果　脑梗死患者急性期血浆uPA和uPAR含量分别为 ( 16 6 4± 384 )ng/L及 ( 1375± 30 3)ng/L ,其他疾病对照组为 ( 10 33± 12 3)ng/L及 ( 978± 12 0 )ng/L ,正常对照组为 ( 10 0 5±12 9)ng/L及 ( 90 5± 15 9)ng/L。脑梗死组与后两组比较P <0 0 5或P <0 0 1。脑梗死患者恢复期uPA含量为 ( 1186± 385 )ng/L ,与两对照组比较P >0 0 5 ,uPAR含量为 ( 115 9± 2 6 1)ng/L ,明显高于两对照组 (均P <0 0 1)。重度患者急性期血浆uPA和uPAR含量分别为 ( 1939± 2 5 7)ng/L及 ( 15 11± 379)ng/L ,中度患者分别为 ( 15 94± 2 0 5 )ng/L及 ( 12 97± 15 1)ng/L ,轻度患者分别为 ( 135 9± 176 )ng/L及 ( 12 2 7± 98)ng/L ,重度患者组与后两组比较P <0 0 1;恢复期uPA和uPAR含量分别为 ( 115 3± 170 )ng/L及( 1186± 15 8)ng/L ,轻度患者分别为 ( 10 4 2± 187)ng/L及 ( 10 5 4± 10 9)ng/L ,两者比较P <0 0 5和     

血管紧张素转换酶抑制剂对慢性心力衰竭患者脑钠肽和去甲肾上腺素的作用

目的探讨不同剂量血管紧张素转换酶抑制剂(ACEI)对慢性心力衰竭患者脑钠肽和去甲肾上腺素(NE)的作用,以及较大剂量ACEI治疗的可行性与安全性。方法将66例慢性心力衰竭患者随机分为培哚普利较小剂量组(33例,2～4mg/d)和较大剂量组(33例,8～10mg/d)治疗12周,治疗前后测定各项指标[NE、脑钠肽浓度,左室舒张末内径(LVED),左室射血分数(LVEF)等]。并且选择30名年龄相仿的健康对照者,分别测定基础NE、脑钠肽浓度。结果慢性心力衰竭患者血浆中脑钠肽浓度随着纽约心脏病协会心功能分级增加而升高,与LVEF呈显著负相关(r=-0.327,P=0.012);脑钠肽与LVED和NE呈显著正相关(r=0.42,P=0.015;r=0.402,P=0.002)。治疗12周后7例患者因出现不能耐受的咳嗽反应而退出(其中较小剂量组3例,较大剂量组4例),其余59例完成研究。较小剂量组治疗后脑钠肽浓度为8μg/L±4μg/L,NE浓度为387ng/L±211ng/L,较大剂量组治疗后脑钠肽浓度为6μg/L±4μg/L,NE浓度为250ng/L±63ng/L,较大剂量组治疗后的脑钠肽、NE浓度明显低于较小剂量组治疗后(均P<0.05)。结论心力衰竭时血浆脑钠肽浓度与心力衰竭严重程度密切相关,且与NE浓度呈正相关。在慢性心力衰竭患者中采用小剂量逐渐递增剂量方式给予培哚普利可明显降低脑钠肽、NE,且耐受性良好。     

异丙肾上腺素对高血压患者单核细胞分泌白细胞介素6及肿瘤坏死因子α的影响

目的:观察异丙肾上腺素(isoproterenol, ISO)对高血压患者单核细胞分泌肿瘤坏死因子α(tumor necrosis factor-alpha ,TNF-α)及白细胞介素6(interleukin-6, IL-6)的影响.方法:选取17例健康志愿者和6例原发性高血压病患者(Ⅰ期)的静脉血样,分离得到单核细胞,用脂多糖(lipopolysaccharide,LPS)刺激细胞后,检测在有或无ISO存在条件下细胞上清液中TNF-α和IL-6含量.结果:(1)在LPS刺激下,高血压组单核细胞分泌TNF-α量较健康对照组显著增加[(1 897±393) ng/L vs. (975±473) ng/L, P＜0.01],但IL-6的分泌在两组间的差异无统计学意义[(5 532±796) ng/L vs. (6 092±2 249) ng/L];(2)在健康对照组和高血压组中,ISO能剂量依赖性抑制LPS引起的单核细胞TNF-α分泌,但对IL-6的分泌则无显著影响;(3)在Ⅰ期高血压患者的单核细胞中,ISO对TNF-α产生的抑制作用与健康对照组相比,差异无统计学意义(P》0.05),给予β肾上腺素受体拮抗剂普萘洛尔可拮抗这种效应.结论:β肾上腺素受体激动可抑制LPS引起单核细胞分泌TNF-α,而对IL-6的分泌无影响,这种抑制效应在Ⅰ期高血压病患者与健康志愿者之间差异无统计学意义.     

肿瘤坏死因子-α基因多态性在重症急性胰腺炎患者中的意义

目的　观察肿瘤坏死因子 (TNF α)基因启动子区域中 - 30 8基因多态性即TNF2及外周血浆TNF α、TNF受体浓度与重症急性胰腺炎 (ASP)及其并发症———严重脓毒症之间的关系。方法　本研究组包括 72例ASP患者和 74个正常人 ,采用聚合酶链反应 (PCR)、NcoI消化及电泳技术检测其多态性。ASP患者血浆TNF α、可溶TNF受体 (sTNF RⅠ和sTNF RⅡ )浓度检测用EASIA法。结果　(1)TNF2出现的频率在ASP组为 2 1例 (2 9 2 % ) ,对照组为 19例 (2 5 7% ) ,两组差异无显著意义 (P>0 0 5 )。ASP组有 2 6例并发严重脓毒症 ,TNF2出现频率 12例 (46 2 % ) ;而无严重脓毒症组为 9例(19 6 % )。TNF2出现的频率在严重脓毒症组显著高于无并发严重脓毒症组 (P <0 0 5 )。 (2 )在严重脓毒症组 ,血浆基础TNF α、sTNF RⅠ和sTNF RⅡ浓度分别为 36± 30 (ng/L)、5 4± 3 5、11 2± 7 9(μg/L) ,无并发严重脓毒症病人分别为 30± 2 5 (ng/L) ,4 6± 3 8、8 8± 6 6 (ng/L) ,两组比较差异均无显著意义 (P >0 0 5 )。 (3)重症胰腺炎患者中 ,TNF2组血浆基础TNF α浓度为 37± 31(ng/L) ,TNF1组为 31± 2 5 (ng/L) ,两组差异无显著意义 (P >0 0 5 )。结论　TNF2与ASP的发生无关 ,但与其导致的严重脓毒症的易感性有关。血浆基础T     

Changes of plasma immuno-reactive beta-endorphin content in patients with congestive heart failure and their clinical significance.

Immunoreactive beta-endorphin (ir-beta-EP) content in plasma was measured by radioimmunoassay in 101 cardiac patients and 30 normal subjects. The results showed that plasma ir-beta-EP levels in patients of Class II (New York Heart Association Classification), Class III and Class IV were significantly higher than those in the normal group and those in patients of Class I (43.14 +/- 2.80, 54.25 +/- 4.47, 79.28 +/- 8.96 ng/L vs 24.23 +/- 2.13, and 24.98 +/- 3.35 ng/L, respectively, P less than 0.01). Plasma concentration of ir-beta-EP in patients complicated with atrial fibrillation was significantly higher than that in patients without atrial fibrillation (56.27 +/- 4.13 vs 44.66 +/- 3.41 ng/L, P less than 0.05). Ir-beta-EP contents in plasma were correlated positively to the cardiothoracic ratios (r = 0.63, P less than 0.001) and PEP/LVET ratios (r = 0.33, P less than 0.01), and were correlated negatively to the left ventricular ejection fraction and axis shortening (r = -0.41 and r = -0.39, P less than 0.001). These results indicated that plasma ir-beta-EP content may serve as a parameter in evaluating cardiac dysfunction.

     

两种途径输注前列腺素E1对肝缺血再灌注损伤保护作用的比较

目的：比较两种途径输注前列腺素E1对肝缺血再灌注损伤的保护作用,寻找最佳途径。方法：20只SD大鼠随机分为两组,在行肝左叶血流阻断及解除阻断同时,门静脉组经门静脉输注PG E1;外周组经股静脉输注PGE1。测定肝血流阻断45min再灌注1h后各组的ALT、AST、LDH值,观察缺血肝叶光镜、电镜下的病理变化及干、湿重量比。结果：门静脉组能明显改善肝功能,与外周静脉组比较有显著差异。外周静脉组缺血肝叶病理学检查见肝细胞呈点片状水肿,核膜有变形;门静脉组肝组织损害不明显。结论：经门静脉输注PGE1是一种新的、安全的对常温下肝缺血再灌注损伤的有效保护方法。     

两种途径输注前列腺素E_1对肝缺血再灌注损伤保护作用的比较

目的 :比较两种途径输注前列腺素E1 对肝缺血再灌注损伤的保护作用 ,寻找最佳途径。方法 :2 0只SD大鼠随机分为两组 ,在行肝左叶血流阻断及解除阻断同时 ,门静脉组经门静脉输注PGE1 ;外周组经股静脉输注PGE1 。测定肝血流阻断 45min再灌注 1h后各组的ALT、AST、LDH值 ,观察缺血肝叶光镜、电镜下的病理变化及干、湿重量比。结果 :门静脉组能明显改善肝功能 ,与外周静脉组比较有显著差异。外周静脉组缺血肝叶病理学检查见肝细胞呈点片状水肿 ,核膜有变形 ;门静脉组肝组织损害不明显。结论 :经门静脉输注PGE1 是一种新的、安全的对常温下肝缺血再灌注损伤的有效保护方法。     

冠脉搭桥围手术期肿瘤坏死因子和内皮素的动态变化及意义

目的观察冠状动脉搭桥手术(CABG)中肿瘤坏死因子-α(TNF-α)和内皮素1(ET-1)的动态变化,探讨其病理意义.方法对32例行冠状动脉搭桥术的病人,分别于术前、麻醉诱导期、阻断升主动脉后、开放升主动脉、手术结束时以及术后2、8、24 h等8个时相采集血样.TNF-α及ET-1血浆浓度应用放射免疫方法进行测定.结果 (1)TNF-α水平在阻断升主动脉后较术前明显升高(18.3 ng/L±3.4 ng/L vs 12.1 ng/L±2.0 ng/L,P<0.05),开放升主动脉后继续上升,并达到峰值(22.4 ng/L±3.6 ng/L),后呈下降趋势,但至术后24 h仍维持在较高水平(18.5 ng/L±4.1 ng/L P<0.05).开放升主动脉后心肺再灌注时TNF-α浓度显著高于阻断升主动脉后未开放前(22.4 ng/L±3.6 ng/L vs 18.3 ng/L±3.4 ng/L P<0.05).(2) ET-1血浆浓度在阻断升主动脉后较术前显著上升 (146 ng/L±20 ng/L vs 97 ng/L±14 ng/L,P<0.05).开放升主动脉后下降,术后2 h出现了第二个高峰,达134 ng/L±19 ng/L,后呈下降趋势,至术后24 h降为92 ng/L±18 ng/L.结论 CABG手术中,减轻TNF-α介导的炎症反应是围术期心肺保护的重要策略.CABG围术期血浆ET-1水平升高可能与手术操作和缺血再灌注损伤有关.     

趋化因子及其受体表达与系统性红斑狼疮临床特征相关性研究

目的研究趋化因子及受体变化与系统性红斑狼疮(SLE)临床特征的相关性。方法采用ELISA法检测37例初发SLE患者和20例正常对照的巨噬细胞炎症蛋白(MIP)-1α、巨噬细胞炎症蛋白(MIP)-1β、激活正常T细胞表达和分泌因子(RANTES)的血清水平,用流式细胞术检测其中18例初发SLE患者及10例正常对照外周血CD4+T细胞表面趋化因子受体CCR1、CCR3、CCR5的表达情况,分析它们的变化与不同临床特征的相关性。结果SLE伴发热患者血清MIP-1α浓度为(52±27)ng/L,体温正常的SLE患者为(28±19)ng/L,差异有统计学意义(P<0·01);SLE伴关节炎患者血清MIP-1β浓度为(221±158)ng/L,不伴关节炎患者为(95±83)ng/L,差异有统计学意义(P<0·01);血清RANTES浓度在血小板减少的SLE患者中为(130±122)ng/L,血小板正常患者为(212±114)ng/L,差异有统计学意义(P<0·05);抗RNP抗体阳性的SLE患者外周血CD4+T细胞中CD4+CCR3+细胞亚群百分率为(14·8±3·0)%,抗RNP抗体阴性患者为(11·3±2·6)%,差异有统计学意义(P<0·05)。结论不同的趋化因子及受体表达异常可能与系统性红斑狼疮系统不同临床特征有关。     

藏族原发性高血压的遗传学研究

目的　探讨遗传因素在藏族原发性高血压 (EH)发病中的作用 ,以及血管紧张素Ⅱ的惟一前体物血管紧张素原 (AGT)基因变异是否参与EH发病。方法　以藏族 35 3例EH患者和 317名正常血压对照者为对象进行病例 对照相关研究。根据相似家系结构的指示对照和指示病例 1∶1配比分析 ,按Falconer公式计算藏族EH的遗传度。以聚合酶链反应 (PCR)和PCR产物的限制性片段长度多态性分析方法 ,分析AGT基因M2 35T多态性和 5′调控区 6A→G变异与藏族EH遗传易感的相关性。结果　 (1)藏族EH先证者 (指示病例 )一级亲属受累率为 43.3% ,EH遗传度为 77.2 %± 13 3%。(2 )EH患者血浆肾素活性 (μg·L-1·h-1)为 1.95± 0 .11,血管紧张素Ⅱ水平 (ng/L)为 72 .6± 4.6 ,均明显高于对照组 (分别为 1.5 9± 0 .11和 5 1.7± 4.6 ,P <0 .0 5 )。 (3)EH组AGT基因 5′调控区 6G等位基因频率 (0 .36 )明显高于对照组 (0 .2 7) (χ2 =9.35 ,P <0 .0 1) ,并与血管紧张素Ⅱ水平呈弱相关 ,而M2 35T多态性与EH易感无明显相关 (P >0 .0 5 )。结论　遗传因素在藏族EH发病中起重要作用 ,AGT基因可能是其重要易感基因之一