螺内酯对慢性心力衰竭患者肾素-血管紧张素-醛固酮系统及脑利钠肽的影响

目的:探讨螺内酯对慢性心力衰竭患者肾素-血管紧张素-醛固酮系统(RAAS)及脑利钠肽(BNP)的影响。方法:将我院收治的90例慢性心力衰竭患者(心功能Ⅱ～Ⅳ级),随机均分为对照组和螺内酯组。对照组给予常规治疗,螺内酯组在对照组基础上给予螺内酯(20 mg,qd,6个月)治疗。于治疗前、治疗后6个月分别检测血清RAAS活性、BNP、血K+及血清醛固酮(ALD)水平。结果:与治疗前比较,螺内酯组治疗后血浆肾素(PRA)、血浆血管紧张素Ⅱ(AngⅡ)无显著变化,而ALD明显降低(P<0.05);与治疗前和对照组治疗后比较,螺内酯组BNP水平明显降低(P<0.01),血K+水平升高(P>0.05)。结论:小剂量螺内酯通过拮抗ALD和降低BNP对改善慢性心力衰竭患者发挥作用,有效控制患者RAAS和BNP水平。     

氢氯噻嗪联用螺内酯长期治疗对RAAS活性和生化指标的影响

目的:探讨氢氯噻嗪(HCTZ)与螺内酯长期联合治疗对高血压患者肾素-血管紧张素-醛固酮系统(RAAS)活性及生化指标的影响。方法:采用多中心研究,选择9所开滦矿区医院,筛选出轻、中度高血压患者。在2周的洗脱期和6周(HCTZ,12.5mg,qd)导入期后,服用HCTZ+螺内酯治疗5a。于洗脱期末和6周HCTZ导入期末、治疗2a、5a检测RAAS活性,每年检测血生化指标。比较各时间点RAAS活性变化与生化指标变化。结果:6周HCTZ导入期末,患者血浆血管紧张素Ⅱ(AngⅡ)和醛固酮(ALD)浓度较基线值显著升高(P<0.01),血钾浓度下降,差异有统计学意义(P<0.05);治疗2a时血浆AngⅡ和ALD浓度已恢复至基线水平;治疗5a后血糖、AngⅡ、ALD浓度变化与基线值比较差异无统计学意义,而血钾和血钠下降(P<0.01)。结论:长期合用HCTZ与螺内酯治疗后RAAS活性可恢复至治疗前水平,对血糖浓度影响不大,而血钾、血钠降低。     

肾血管性高血压和肾上腺腺瘤患者肾素-血管紧张素-醛固酮含量分析

目的 探讨肾素-血管紧张素-醛固酮系统、内皮素、一氧化氮在肾血管性高血压患者、肾上腺腺瘤患者中的作用和意义.方法 采用放射免疫分析的方法测量肾血管性高血压组(40例)、肾上腺腺瘤组(35例)和健康对照组(35例)血清肾素、血管紧张素Ⅱ、醛固酮、内皮素含量,用酶免疫法测定上述人群一氧化氮合酶(NOS)的含量来表示NO的量.结果 肾血管性高血压患者肾素、血管紧张素、醛固酮、内皮素含量高于健康对照组(P＜0.01),NOS含量低于健康对照组(P＜0.05);肾上腺腺瘤组醛固酮和内皮素含量高于健康对照组(P＜0.01),肾素、血管紧张素低于健康对照组(P＜0.05).结论 肾索、血管紧张素、醛固酮、内皮素和NO的检测可为临床早期诊断肾上腺腺瘤、肾血管性高血压提供依据.     

不同时间给予比索洛尔对非杓型原发性高血压患者肾素-血管紧张素-醛固酮系统的影响

目的:探讨不同时间给予比索洛尔对非杓型原发性高血压患者肾素-血管紧张素-醛固酮系统(RAAS)的影响。方法:选择非杓型原发性高血压病患者60例,采取随机平行对照试验,观察比索洛尔每日早晨(8?00)给药2.5～10 mg、比索洛尔每日夜间(20?00)给药2.5～10 mg治疗8周前后分别检测血浆肾素(Ren)、血管紧张素Ⅱ(AngⅡ)、醛固酮(Ald)浓度并进行分析评价。结果:治疗后上述各指标较治疗前均明显降低,差异有统计学意义(P<0.05)。两组间比较肾素指标无统计学差异(P>0.05),血管紧张素Ⅱ、醛固酮指标有统计学差异(P<0.05)。结论:早晨或夜间服用比索洛尔均能降低患者肾素、血管紧张素Ⅱ和醛固酮浓度,晚上服用比索洛尔对血管紧张素Ⅱ和醛固酮的影响更为显著。     

作用于RAAS的抗高血压药研究进展

综述作用于肾素 -血管紧张素 -醛固酮系统 (RAAS)的抗高血压药研究进展 ,分别介绍血管紧张素转化酶抑制剂、血管紧张素Ⅱ受体拮抗剂及肾素和醛固酮抑制剂的药理作用、不良反应以及若干目前临床常用或正在研发中的相应药物及其特点。作用于RAAS药物的研发为治疗高血压提供了更多的选择。     

氢氯噻嗪对高血压患者肾素-血管紧张素-醛固酮系统及生化指标的影响

目的:观察不同剂量氢氯噻嗪(HCTZ)对原发性高血压患者肾素-血管紧张素-醛固酮系统(RAAS)活性及生化指标的影响。方法:选择2009年1月-2010年7月在我院治疗的120例轻、中度高血压患者,随机分为3组:对照组(A组)、HCTZ12.5mg组(B组)和HCTZ25.0mg组(C组)。A组:给予苯磺酸氨氯地平5mg,口服,qd;B组:在A组基础上加用HCTZ12.5mg,口服,qd;C组:在A组基础上加用HCTZ25.0mg,口服,qd。6周后比较各组患者血清RAAS活性和生化指标。结果:B组的血管紧张素Ⅱ(AngⅡ)和醛固酮(ALD)浓度较A组高(P<0.05),血钾、血钠浓度下降不明显,血糖未见明显变化(P>0.05);C组血浆肾素(PRA)、AngⅡ和ALD较B组高(P<0.05),血钾、血钠浓度下降,血糖增高。结论:12.5mg的HCTZ即能激活RAAS活性,25.0mg的HCTZ对生化指标有较大影响。     

心房颤动患者血清半胱氨酸蛋白酶抑制剂C变化及其与肾素-血管紧张素-醛固酮系统的关系

目的 探讨持续性心房颤动(CAF)患者血清半胱氨酸蛋白酶抑制剂C(CysC)水平的变化及其与肾素-血管紧张素-醛固酮系统(RAAS)的关系.方法 将103例符合入选标准的患者分为CAF组53例和对照组50例.比较2组血清CysC、肾素(PRA)、血管紧张素Ⅱ(Ang Ⅱ)、醛固酮(Ald)水平.结果 与对照组比较,CAF组血清CysC、PRA、AngⅡ、Ald水平均明显升高(P＜0.01);且CAF组血清CysC水平与PRA、Ang Ⅱ、Ald水平呈显著正相关(r分别为0.515、0.489、0.449).结论 CAF患者血清CysC水平明显升高,与其RAAS的激活密切相关.     

糖代谢异常患者血浆醛固酮水平变化的临床意义

目的观察高血糖、高血压患者中肾素-血管紧张素蹙固酮（renin-angiotensin-aldosterone,RAA）水平,探讨是否RAAS的激活是2者共同的发病机制。方法用放射免疫分析法测定106例正常人、112例单纯糖代谢异常患者、101例单纯原发性高血压患者及127例糖代谢异常合并原发性高血压患者的血浆RAA水平和活性。结果3组醛固酮水平均明显高于CON组,差异有统计学意义（P〈0．01）,I-IGM常组中血管紧张素Ⅱ水平明显高于其他各组,差异有统计学意义（P〈0．01）,各组间肾素活性差异无统计学意义。血浆醛固酮水平与空腹血糖、肾素、收缩压、血管紧张素Ⅱ高度相关。结论高血糖和原发性高血压同样存在RAAS的激活,组织水平干预醛固酮应该成为血糖代谢异常患者的一个治疗目标。     

局部肾素-血管紧张素-醛固酮系统与糖尿病肾病的治疗

循环中肾素-血管紧张素-醛固酮系统(RAAS)成分由分布于全身的组织细胞合成与分泌.糖尿时,肾脏局部肾素、血管紧张素(Ang)Ⅱ、醛固酮等活性增加,它们作用于血管或通过激活炎症因子等途径,导致肾血管病变及肾纤维化.动物试验与临床研究表明,抑制RAAS可延缓糖尿病肾病进程.     

肾素-血管紧张素-醛固酮系统抑制剂多靶点干预治疗高血压的研究进展

肾素-血管紧张素-醛固酮系统(RAAS)是参与高血压发病和维持不可或缺的环节;RAAS抑制剂治疗高血压被临床广泛应用,其中主要包括直接肾素抑制剂、血管紧张素转换酶抑制剂和血管紧张素受体拮抗剂.它们作用于RAAS不同靶点,对RAAS抑制剂有效性的影响及其临床应用地位和意义一直被人们所关注,因此对三者各靶点作用特点的进行总结,以揭示RAAS抑制剂多靶点干预的重要性和意义.     

Nachweis einiger Heilmittel in der Kniegelenksynovialflüssigkeit

Zusammenfassung Mittels Gaschromatographie und Dünschichtchromatographie wiesen die Autoren 11 Substanzen nach, welche durch Injektion oder nach Verabreichung per os in die Kniegelenksynovialflüssigkeit eindrangen. In ihrer Aufstellung konnten sie eine direkte Beziehung zwischen Struktur sowie chemischphysikalischen Eigenschaften der Substanz und ihrer Fähigkeit, aus dem Blut in die Kniegelenksynovialflüssigkeit einzudringen, nicht nachweisen, außer der Tatsache, daß Substanzen mit starker Affinität zu Eiweißstoffen erst in höheren Dosen nachweisbar waren.     

Synthesis,Cytotoxicity and Antileishmanial Activity of Some N-(2-(indol-3-yl)ethyl)-7-chloroquinolin-4-amines

We report herein the condensation of 4,7-dichloroquinoline (1) with tryptamine (2) and D-tryptophan methyl ester (3) . Hydrolysis of the methyl ester adduct (5) yielded the free acid (6) . The compounds were evaluated in vitro for activity against four different species of Leishmania promastigote forms and for cytotoxic activity against Kb and Vero cells. Compound (5) showed good activity against the Leishmania species tested, while all three compounds displayed moderate activity in both Kb and Vero cells.     

Emerging drugs for epilepsy

Epilepsy affects ≤ 1% of the world's population. Antiepileptic drugs (AEDs) are the mainstay of treatment, although more than a third of patients are not rendered seizure free with existing medications. Uncontrolled epilepsy is associated with increased mortality and physical injuries, and a range of psychosocial morbidities, posing a substantial economic burden on individuals and society. Limitations of the present AEDs include suboptimal efficacy and their association with a host of adverse reactions. Continued efforts are being made in drug development to overcome these shortcomings employing a range of strategies, including modification of the structure of existing drugs, targeting novel molecular substrates and non-mechanism-based drug screening of compounds in traditional and newer animal models. This article reviews the need for new treatments and discusses some of the emerging compounds that have entered clinical development. The ultimate goal is to develop novel agents that can prevent the occurrence of seizures and the progression of epilepsy in at risk individuals.     

盐酸达泊西汀中甲磺酸甲酯、甲磺酸乙酯及甲磺酸异丙酯的顶空毛细管GC-ECD法测定

建立了衍生化顶空毛细管气相色谱-电子捕获检测器(ECD)法测定盐酸达泊西汀中的甲磺酸甲酯(MMS)、甲磺酸乙酯(EMS)和甲磺酸异丙酯(IMS).应用碘化钠衍生技术,使用PW-5毛细管柱,载气为氮气,ECD检测,程序升温.MMS、EMS和IMS分别在0.03～0.30、0.05～0.50和0.05～0.50 μg/ml浓度范围内线性关系良好,平均回收率分别为63.5％、100.3％和96.2％,最低检测限分别为0.30、0.50和0.50 ng/ml.     

Lung disease and PKCs

The lung offers a rich opportunity for development of therapeutic strategies focused on isozymes of protein kinase C (PKCs). PKCs are important in many cellular responses in the lung, and existing therapies for pulmonary disorders are inadequate. The lung poses unique challenges as it interfaces with air and blood, contains a pulmonary and systemic circulation, and consists of many cell types. Key structures are bronchial and pulmonary vessels, branching airways, and distal air sacs defined by alveolar walls containing capillaries and interstitial space. The cellular composition of each vessel, airway, and alveolar wall is heterogeneous. Injurious environmental stimuli signal through PKCs and cause a variety of disorders. Edema formation and pulmonary hypertension (PHTN) result from derangements in endothelial, smooth muscle (SM), and/or adventitial fibroblast cell phenotype. Asthma, chronic obstructive pulmonary disease (COPD), and lung cancer are characterized by distinctive pathological changes in airway epithelial, SM, and mucous-generating cells. Acute and chronic pneumonitis and fibrosis occur in the alveolar space and interstitium with type 2 pneumocytes and interstitial fibroblasts/myofibroblasts playing a prominent role. At each site, inflammatory, immune, and vascular progenitor cells contribute to the injury and repair process. Many strategies have been used to investigate PKCs in lung injury. Isolated organ preparations and whole animal studies are powerful approaches especially when genetically engineered mice are used. More analysis of PKC isozymes in normal and diseased human lung tissue and cells is needed to complement this work. Since opposing or counter-regulatory effects of selected PKCs in the same cell or tissue have been found, it may be desirable to target more than one PKC isozyme and potentially in different directions. Because multiple signaling pathways contribute to the key cellular responses important in lung biology, therapeutic strategies targeting PKCs may be more effective if combined with inhibitors of other pathways for additive or synergistic effect. Mechanisms that regulate PKC activity, including phosphorylation and interaction with isozyme-specific binding proteins, are also potential therapeutic targets. Key isotypes of PKC involved in lung pathophysiology are summarized and current and evolving therapeutic approaches to target them are identified.