苯那普利对高血压病患者血浆内皮素及一氧化氮的影响

目的 :探讨苯那普利对高血压病 (EH)患者血浆内皮素 (ET)及一氧化氮 (NO)的影响。方法 :观察苯那普利 (5～ 2 0 mg,每日 1次口服 4周 )治疗的 30例 EH患者治疗前后血浆 ET、NO水平 ,并与 2 8例健康者血浆 ET、NO对照。结果 :EH患者 ET较对照组显著升高 (P <0 .0 1) ,NO显著降低 (P<0 .0 1)。经苯那普利治疗后 ,收缩压、舒张压都有显著性下降 (P<0 .0 1) ,ET显著下降(P <0 .0 1) ,NO显著升高 (P <0 .0 1)。结论 :苯那普利不仅有较好的降压作用 ,还能有效地恢复血浆 ET、NO的代谢水平     

非洛地平对原发性高血压病患者血管内皮功能失调逆转作用的研究

目的:探讨非洛地平[商品名:波依定,阿斯特拉(无锡)制药有限公司生产]对原发性高血压病(EH)患者血浆内皮素(ET)及一氧化氮(NO)的调节作用。方法:选择40例EH患者,用非洛地平5～10mg,每日一次,连服4周观察治疗前后血浆ET、NO水平,并与30例健康者血浆ET、NO对照。结果:EH患者ET较对照组显著升高(P<0.01),NO显著降低(P<0.01)。经非洛地平治疗后,收缩压、舒张压都有显著下降(P<0.01),ET显著下降(P<0.01),NO显著升高(P<0.05)。结论:非洛地平不仅具有很好的降压作用,还能逆转内皮功能失调。     

非洛地平对原发性高血压患者血浆一氧化氮和内皮素含量的影响

目的探讨原发性高血压(EH)患者血浆一氧化氮(NO)和内皮素(ET)含量的变化及非洛地平对其的影响。方法观察72例EH患者(EH组)非洛地平治疗前后血浆NO和ET水平的变化,并与30例正常人(对照组)进行对比分析。结果非洛地平治疗前EH组血浆NO明显低于对照组(P<0.01),血浆ET明显高于对照组(P<0.01)。非洛地平治疗6周后,EH组血压和血浆ET水平明显降低,NO水平明显增高(P<0.01)。结论非洛地平在有效降血压的同时,能使EH患者血浆NO水平升高,ET水平降低,因此对血管内皮功能具有保护作用。     

左旋氨氯地平对高血压病病人血管内皮功能的影响

目的探讨左旋氨氯地平对高血压病(EH)病人血浆内皮素(ET)及一氧化氮(NO)的影响。方法选择50例EH病人,用左旋氨氯地平(2.5～5.0)mg治疗,每日1次,连服8周,观察治疗前后血浆ET,NO水平,并与40名健康者作比较。结果高血压病病人ET为(69.1±6.3)pg/mL较正常对照组的(44.7±5.5)pg/mL显著升高(P<0.05),NO为(52.3±7.1)μmol/mL较正常对照组的(88.9±8.7)μmol/L显著降低(P<0.05)。经左旋氨氯地平治疗后,收缩压(SBP)、舒张压(DBP)、ET显著下降(P<0.05),NO升高明显(P<0.05)。结论左旋氨氯地平不仅具有很好的降压作用,还能逆转内皮功能不良。     

老年非杓型高血压患者血浆一氧化氮内皮素神经肽Y水平及氨氯地平对其影响

目的 :探讨老年非杓型高血压 ( EH)患者血浆内皮素 ( ET)、一氧化氮 ( NO)、神经肽 Y ( NPY)及血管紧张素 ( Ang )浓度的变化及氨氯地平对其影响。方法 :测定 4 2例非杓型 EH患者氨氯地平治疗前后血浆ET、NO、NPY、Ang 浓度变化 ,并与杓型 EH患者及健康老年人进行对照。结果 :老年非杓型 EH患者血浆 ET、NPY、Ang 水平明显高于老年杓型 EH患者 ,杓型及非杓型 EH组 NO水平低于正常对照。氨氯地平能明显降低白昼与夜间收缩压及白昼舒张压 ,对夜间舒张压影响较小 ;治疗后非杓型 EH患者血浆 ET、NPY水平下降 ,NO水平升高 ,Ang 水平无显著性改变。结论 :ET、NO、NPY及 Ang 参与了老年非杓型 EH的病理过程 ,氨氯地平是一种治疗老年非杓型 EH患者的有效药物     

2型糖尿病患者血管并发症与血浆内皮素和一氧化氮的相关性及胰激肽释放酶干预治疗的研究

目的　探讨 2型糖尿病患者血管并发症与血浆内皮素 (ET)、一氧化氮 (NO)的相关性及胰激肽释放酶 (TPK)干预治疗对其影响。　方法　随机选择 2型糖尿病患者 1 82例及正常对照 4 0名。放射免疫分析测定 (RIA)及酶连免疫吸附测定 (EL ISA)检测血浆 ET、NO水平和 TPK干预治疗后各指标的变化。　结果　 2型糖尿病患者血浆 ET较正常人显著升高 (P<0 .0 1 ) ,伴血管并发症患者较单纯 2型糖尿病患者血浆 ET水平显著升高 (P<0 .0 1 )。 2型糖尿病血管并发症组较单纯 2型糖尿病组及正常对照组血浆 NO水平显著降低 (P<0 .0 1 )。2型糖尿病患者经 TPK干预治疗后血浆 ET水平降低 ,NO水平升高 ,尿白蛋白排泄率降低 ,血液流变学有所改善。　结论　内皮系统功能紊乱参与了 2型糖尿病血管并发症的发生。 TPK干预治疗可以改善 2型糖尿病患者内皮系统功能 ,防治糖尿病血管并发症的发生、发展     

缬沙坦和美托洛尔对老年高血压患者血浆内皮素和一氧化氮的影响

目的 了解缬沙坦和美托洛尔对老年高血压患者血浆内皮素(ET)、一氧化氮(NO)的影响. 方法 将67例老年高血压患者随机分为2组,分别服缬沙坦和美托洛尔治疗8周,观察服药前后血压及血浆ET、NO的变化. 结果 治疗后2组血压明显下降(P<0.01),以缬沙坦组下降较为显著;缬沙坦组血浆ET明显下降(P<0.01),NO显著升高(P<0.01),而美托洛尔组血浆ET及NO无明显改变. 结论 缬沙坦不仅有良好的降压作用.同时有较好的血管内皮保护功能.     

高血压患者血管活性物质水平变化及雷米普利干预的影响

目的 :本研究主要了解原发性高血压 (EH)不同时期血浆肾上腺髓质素N端 2 0肽 (PAMP)、内皮素 (ET)、血管紧张素Ⅱ (AⅡ )、肾上腺素 (E)和去甲肾上腺素 (NE)浓度变化及雷米普利对其影响。方法 :40例EH患者应用雷米普利治疗前后和 2 0例正常对照组检测上述血管活性物质水平 ,血浆PAMP、ET和AⅡ的放免活性用放射免疫法测定 ,血浆E和NE浓度用高压液相法测定。结果 :EH患者不同时期血浆PAMP、ET、AⅡ、E和NE水平均明显高于对照组 (P <0 0 5～ <0 0 1) ;并随病期进展而增加(P均 <0 0 5 ) ;与平均动脉压 (MAP)均呈正相关 (r =0 431、0 82 1、0 76 2、0 46 7、0 473,P <0 0 5～ <0 0 0 1) ;PAMP与ET、AⅡ、E、NE水平亦有良好的相关性 (r =0 5 31、0 5 2 4、0 40 1、0 42 5 ,P <0 0 5～ <0 0 1) ;雷米普利治疗 4周 ,血压下降同时伴血浆血管活性物质浓度改变。结论 :高血压的发生和发展与上述缩血管活性物质水平变化有关 ;舒血管肽PAMP浓度升高是维持机体内环境稳定的一种代偿性保护机制 ;雷米普利在降压同时能改变其血管活性物质浓度水平     

高血压不同并发症患者血浆内皮素变化及辛伐他汀干预对其影响

目的 了解原发性高血压(EH)不同合并症患者血浆内皮素(ET)浓度的变化及辛伐他汀干预对其影响.方法 入选EH患者149例,根据合并症的不同分为单纯EH组44例,EH合并左心室肥厚(EH-LVH)组40例,EH合并心房颤动(EH-AF)组36例,EH合并腔隙性脑梗死(EH-LI)组29例,同时选择30例健康体检者作为对照.149例EH患者按血压水平随机分为常规治疗组(主要应用钙拮抗剂、血管紧张素转换酶抑制剂、利尿剂、β受体阻滞剂等药治疗8周)和辛伐他汀干预组(常规治疗+辛伐他汀40 mg/d),药物治疗前后检测血浆内皮素.结果 (1)EH组ET浓度高于对照组[(71.42±6.62)pg/ml对(45.52±8.28)pg/ml,P<0.01]并与血压升高程度呈正相关(r=0.746,P<0.001),EH-LVH组、EH-AF组、EH-LI组ET浓度均高于EH组[(97.67±10.53)pg/ml、(102.15±12.96)pg/ml、(103.49±9.91)pg/ml对(71.42±6.62)pg/ml,P<0.01],ET浓度变化均与血压升高程度呈正相关(r=0.671,r=0.592,r=0.530,P均<0.001).(2)EH-AF组左心房内径与ET浓度呈正相关(r=0.684,P<0.001);EH-LVH组的左心室质量指数与ET浓度呈正相关(r=0.545,P<0.001).(3)EH-LVH组、EH-AF组、EH-LI组的3级高血压所占的百分比均高于EH组.(4)EH 3级辛伐他汀干预组治疗后血压水平较常规治疗组下降更为显著(P<0.05).(5)EH 2级辛伐他汀干预组治疗后ET水平较常规治疗组显著降低(P<0.05),EH 3级辛伐他汀干预组和常规治疗组治疗后ET水平均显著降低(P<0.05),但辛伐他汀干预组下降更为显著(P<0.05).结论 ET水平与EH的严重程度呈正相关,辛伐他汀干预能更显著降低EH患者ET水平和EH3级患者的血压,提示对EH患者在使用降压药物控制血压的同时合用他汀类药物可能更有益.     

老年男性高血压病与中医肾虚血瘀证相关性研究

目的　探讨老年高血压病与中医肾虚血瘀证的客观联系 ,进一步研究血瘀证和老年肾虚的微观机理。方法　以病证结合方式 ,选取66例高血压病男性患者 ,观察老年高血压病患者性激素、内皮细胞功能的变化规律。结果　老年男性高血压病与同龄正常对照组相比 ,血浆 ET含量明显升高 (P<0 .0 5) ,ET/ NO比值更有显著性意义 (P<0 .0 1 ) ;血浆 E2 含量明显增加 (P<0 .0 5) ,E2 / T比值显著增高。高血压患者的 E2 / T水平与ET/ NO比值直线相关分析呈显著正相关 (r=0 .71 ,P<0 .0 5)。结论　随着主导性激素水平的降低 ,血管内皮细胞功能损害加重 ,ET- NO分泌失衡 ,导致血管收缩、血液凝聚 ,促进血栓形成 ,是高血压病易于并发心、脑血栓性疾病的本质所在 ,中老年高血压病以肾虚为本、血瘀为标     

Anti-malarial efficacy of pyronaridine and artesunate in combination in vitro and in vivo

Pyronaridine is a Mannich base anti-malarial with demonstrated efficacy against drug resistant Plasmodium falciparum, P. vivax, P. ovale and P. malariae. However, resistance to pyronaridine can develop quickly when it is used alone but can be considerably delayed when it is administered with artesunate in rodent malaria models. The aim of this study was to evaluate the efficacy of pyronaridine in combination with artesunate against P. falciparum in vitro and in rodent malaria models in vivo to support its clinical application. Pyronaridine showed consistently high levels of in vitro activity against a panel of six P. falciparum drug-sensitive and resistant strains (Geometric Mean IC50=2.24 nM, 95% CI=1.20-3.27). In vitro interactions between pyronaridine and artesunate showed a slight antagonistic trend, but in vivo compared to pyronaridine and artesunate administered alone, the 3:1 ratio of the combination, reduced the ED90 of artesunate by approximately 15.6-fold in a pyronaridine-resistant P. berghei line and by approximately 200-fold in an artesunate-resistant line of P. berghei. Complete cure rates were achieved with doses of the combination above or equal to 8 mg/kg per day against P. chabaudi AS. These results indicate that the combination had an enhanced effect over monotherapy and lower daily doses of artesunate could be used to obtain a curative effect. The data suggest that the combination of pyronaridine and artesunate should have potential in areas of multi-drug resistant malaria.     

Modulation of enterotoxin binding and function in vitro and in vivo

The use of the nontoxic B subunits of cholera and Escherichia coli enterotoxins in vitro and in vivo led to a decrease in toxin binding to target cells and a decrease in toxin-induced effects (i.e., morphological effects, adenylate cyclase activation, and fluid secretion). The reduction in toxin binding involves a process of down-regulation of cellular receptors for the toxin and not toxin occupancy of receptors. The extent of inhibition was dependent on the amount of B subunit used and on the duration of time after its use. Thus, in vivo exposure to a single bolus of B subunit was sufficient to block toxin binding and activity for up to 18 h. Because the B subunit binds extensively to the esophagus and the stomach, peroral administration will require a preparation that allows the subunit to reach the small bowel in a protected form. Our data provide a rationale for using B subunit therapy for short-term protection against the effects of enterotoxins, before the development of an immune response.     

我国高血压防治现状和策略

<正>我国现患高血压2亿人,由于人群高血压患病率的不断升高和防控力度不够,我国高血压人群的知晓率、治疗率、控制率仍处于较低水平。对于像高血压这样的群体性慢性病,应当采取全人     

Cooperation of B- and T-lymphocytes of the human in vitro and in vivo

It is reported on the experimental proofs for the existence of a cooperation of different populations of lymphocytes in man. Regulatory lymphocytes play a part in the regulation of the synthesis of immunoglobulins by polyclonally stimulated B-lymphocytes, in the generation of killer-T-cells and in the regulation of the DNA-synthesis by mitogenically stimulated T- and B-cells. Typical helper- and suppressor-effects may be proved. Disturbances of lymphocytic interactions may be a cause for the development of immune deficiency diseases. It is very probable that also in several chronic infections a dysfunction of regulatory T-lymphocytes is present.     

Uptake of labeled alloxan in mouse organs and mitochondria in vivo and in vitro

[14C]2-Alloxan was administered in vivo and in vitro for study of the uptake of alloxan in different organs and their mitochondia of mice. After in vivo administration, radioactivity was demonstrated in all organs investigated, with quantitative differences: endocrine pancreas greater than liver greater than exocrine pancreas and heart. No significant difference was found between the iv and ip routes of injection. An in vivo uptake of alloxan was also found in mitochondria, with significant quantitative differences as to the origin of the organelles: endocrine pancreas greater than liver greater than exocrine pancreas and heart. Pretreatment with D-glucose caused significantly decreased uptake in liver, exocrine pancreas, and heart, but significantly increased uptake in endocrine pancreas, whereas the uptake was significantly decreased in the mitochondria from all of these organs. In vitro uptake was observed in all kinds of mitochondria studied. This uptake was higher than the in vivo uptake in mitochondria from liver, exocrine pancreas, and heart, whereas the uptake in vivo was higher than the in vitro uptake in islet mitochondria. The presence of D-glucose did not affect the in vitro uptake of alloxan in mitochondria. The findings show that in vivo, alloxan passes across plasma membranes and is taken up by mitochondria, and data obtained with mitochondrial subfractions may also indicate a passage across mitochondrial membranes. D-Glucose protection against alloxan diabetogenicity may be associated with prevention of mitochondrial uptake of alloxan. This prevention seems to be dependent on the metabolism of glucose.