心力衰竭时血浆内皮素和血管紧张素Ⅱ变化及药物干预研究

目的探讨心力衰竭患者血浆内皮素（ET）和血管紧张素Ⅱ（AngⅡ）的变化，并观察苯那普利对心衰患儿的疗效。方法40例充血性心力衰竭（CHF）患儿，随机分为苯那普利组（20例）和常规组（20例，其中5例未完成治疗）。用放射免疫法测定血浆ET和AngⅡ，比色法测定血管紧张素转换酶（ACE）水平。常规组用常规抗心衰治疗（洋地黄和利尿剂等），苯那普利组在常规治疗基础上加用苯那普利，治疗4～8周，观察各组治疗效果。结果正常对照组（20人）和40例CHF患儿血浆ET、AngⅡ和ACE水平分别为80．4±19．2ng／L对134．3±47．6ng／L（P＜0．001），96．0±35．5ng／L对223．9±95．5ng／L（P＜0．001），326．8±37．8IU对408．6±67．5IU（P＜0．001）。血浆ET和AngⅡ呈正相关（r＝0．324，P＜0．05）。苯那普利组治疗后ET、AngⅡ和ACE水平均明显下降，而常规组治疗前后均无明显差异。结论CHF患儿血浆ET、AngⅡ和ACE水平均显著高于正常儿童；常规治疗加苯那普利治疗CHF效果明显优于常规治疗。     

紧素血管紧张素系统及血管内皮损伤在小儿心衰中的作用及药物干预研究

３５例心衰患儿分为常治疗组１５例及苯那利加常治疗组２０地治疗前后对照检测血管紧张素Ⅱ、血管紧张素转换酶、内皮素、循环内皮细胞、心胸比率、射血分数、收缩时间新时期、小轴缩短率及左室重量指数。     

血管紧张素转换酶基因多态性与肾脏疾病

肾素-血管紧张素-醛固酮系统(RAAS)是人体内调节血压、水电解质平衡的重要系统之一,在肾脏疾病发生发展中占重要地位。该系统中血管紧张素Ⅰ(AngⅠ)在血管紧张素转换酶(ACE)作用下生成AngⅡ,才能发挥功能,因此ACE是肾素-血管紧张素系统中的关键酶。人体血清ACE水平主要受控于AC     

苯那普利用于儿童抗心力衰竭治疗的临床研究

目的 探讨心力衰竭（简称心衰）患儿血浆内皮素（ＥＴ）和血管紧张素Ⅱ（ＡｎｇⅡ）的变化。并观察苯那普利对心衰串儿的疗效。方法 ４０例充血性心力衰竭（ＣＨＦ）患儿中坚持药物疗程的３５例，分为苯那普利组（２０例）和常规组（１５例）用放射免疫法测定血浆ＥＴ和ＡｎｇⅡ，ｐｅｒｃｏｌｌ密度梯度离心法测定循环内皮细胞（ＣＥＣ），比色法测定血管紧张素转换酶（ＡＣＥ）。常规组用常规抗心衰治疗（洋地黄，利尿剂及血管扩     

单纯性肥胖儿童肾素-血管紧张素系统与心肌肥厚的关系

目的 探讨单纯性肥胖儿童肾素-血管紧张素系统与心肌肥厚的关系。方法 分别对31例单纯性肥胖儿童和31例正常对照组儿童测量其体质指数(BMI)、左室心肌质量(LVM)、血浆血管紧张素Ⅱ(AngⅡ)、及醛固酮(ALD)浓度。结果 1．肥胖组AngⅡ、ALD均显著高于对照组；2．肥胖组LVM显著高于对照组；3．肥胖组中AngⅡ及ALD均与LVM之间存在直线正相关和回归关系。结论 肥胖组儿童存在肾素-血管紧张素-醛固酮系统(RAAS)异常激活，其在引起其心肌肥厚中起作用。     

卡托普利治疗病毒性心肌炎患儿前后血浆血管紧张素Ⅱ和心功能变化

目的　了解病毒性心肌炎 (VM)患儿血浆血管紧张素Ⅱ (AngⅡ )水平和心功能的变化及卡托普利 (CAP)治疗VM的效果。方法　采用放射免疫法测定血浆AngⅡ浓度和多普勒超声心动图检测心功能 ;检测VM组 (n =60 )治疗前、后 (CAP组、常规组及对照组各 30例 )血浆AngⅡ浓度和心功能。结果　 1 .VM患儿血浆AngⅡ水平较对照组明显升高 ,心肌收缩舒张功能明显减退 ,有显著性差异 ,AngⅡ水平与心收缩舒张功能显著相关 ;2 .与治疗前比较两组VM患儿治疗后AngⅡ水平下降 ,心肌收缩功能好转 ,有显著性差异 ,CAP组舒张功能明显好转 ,常规组无明显好转 ;治疗后两组比较 ,CAP组AngⅡ水平和心收缩舒张功能明显好转 ,与常规组比较有显著差异。结论　VM患儿血浆AngⅡ水平明显增高是导致心肌收缩舒张功能减退的重要因素 ;应用CAP治疗VM ,能降低血浆AngⅡ浓度 ,改善心功能。     

血管紧张素转换酶在庆大霉素诱导的大鼠急性肾衰竭中的变化

血管紧张素转换酶（ACE）是肾素-血管紧张素系统（hAS）的关键酶之一,其主要生理功能是将血管紧张素Ⅰ（Ansi）转化为效应肽AngⅡ。肾脏自身存在RAS,AngⅡ具有丝裂原活性,可以促进细胞增殖。急性肾衰竭的恢复伴随着小管细胞的增殖,ACE作为AngⅡ转化酶,其在ARF中的变化及意义报道较少,本研究于2004年5月至12月通过对庆大霉素（GM）诱导的大鼠急性肾衰竭（ARF）肾皮质、血浆、尿液中ACE活性的研究,探讨ACE在ARF中的变化。     

肺炎心衰患儿血管内皮活性因子水平变化及其与PaO2相关性的研究

目的研究肺炎心衰患儿血管内皮活性因子水平变化与动脉血氧分压的关系,探讨心衰的发生机制.方法采用放射免疫分析法和Geriss硝酸盐还原酶两点法测定不同程度肺炎患儿血浆内皮素(ET)、血管紧张素Ⅱ(Ang Ⅱ)、一氧化氮(NO)水平,同时测定动脉血氧分压,并以正常小儿作对照.结果肺炎组血浆ET、Ang Ⅱ、NO升高与正常对照组比较差异有显著性(P＜0.01).肺炎心衰组血浆ET、Ang Ⅱ明显升高,与正常对照组和肺炎组比较均有显著性差异(P＜0.01),血浆NO较正常对照组和肺炎组明显降低(P＜0.01).心衰纠正后,各项指标均不同程度恢复,但仍未恢复到正常范围,与正常对照组比较P＜0.05.肺炎患儿PaO2与血浆ET、Ang Ⅱ及NO无相关性(P＞0.05),肺炎心衰患儿PaO2与血浆ET、Ang H呈负相关(r=-0.73、-0.67,P＜0.01),与血浆NO呈正相关(r=0.71,P＜0.01).结论血管内皮细胞分泌的ET、Ang Ⅱ和NO共同参与了肺炎的病理生理过程,三者相互影响,相互作用,是引起重症肺炎时心力衰竭发生与发展的重要因素之一.     

血管紧张素转换酶抑制剂治疗充血性心力衰竭

血管紧张素转换酶抑制剂(angitension aon-verting enzyme inhibitor,ACEI)治疗充血性心力衰竭(CHF),代表了80年代治疗CHF的新进展。现将ACEI的作用机理、治疗CHF血液动力学改变及其它概述如下。1 ACEI的作用机理认为ACEI主要是通过抑制血管紧张素转换酶(angiotension converting enzyme,ACE),减少血管紧张素Ⅱ(angiotensionⅡ,Ang Ⅱ)而发挥扩血     

内皮素及一氧化氮在肾小球硬化大鼠肾组织的表达及意义(英文)

目的　内皮素 1(ET 1)和一氧化氮 (NO)是否参与了肾小球硬化过程尚缺乏广泛的认识。本实验通过制备阿霉素肾小球硬化大鼠模型并应用血管紧张素转换酶抑制剂 (ACEI)莱那普利和血管紧张素Ⅱ Ⅰ型受体拮抗剂芦沙坦干预 ,观察ET 1和NO在肾小球硬化过程中的变化及作用。方法　大鼠随机分成假手术 (对照 )组(C组 ) ,肾小球硬化组 (D组 ) ,肾小球硬化苯那普利治疗组 (DB组 )和肾小球硬化芦沙坦治疗组 (DL组 ) ,治疗 6周后用RT PCR分别测定肾皮质内皮素 1(ET 1)和诱导型一氧化氮合酶 (iNOS)表达 ,用Westernblotting测定ET 1和iNOS蛋白 ,免疫组化测定肾组织Ⅳ型胶原 (ColⅣ )和纤维连接蛋白 (Fn)。结果　肾小球硬化组出现明显蛋白尿、血白蛋白下降及胆固醇上升和肾小球系膜细胞增生 ,细胞外基质沉积。肾皮质ET 1mRNA和蛋白表达为对照组的 3.5 8倍和 2 .83倍 ,肾皮质iNOSmRNA和蛋白表达为对照组的 4 .2 8倍和 3.15倍 ,肾皮质ColⅣ和Fn表达也明显上调。苯那普利和芦沙坦分别治疗 6周后 ,能明显减轻肾小球硬化的生化改变及病理改变 ,同时下调了ET 1、iNOSmRNA及蛋白表达 ,ColⅣ和Fn水平也降低。结论　ET 1和NO参与了肾小球硬化进展。ET 1andiNOS的抑制阻滞了细胞外基质的沉积 ,从而可以预防肾小球硬化症的发生。     

Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and dichlorodiphenyl dichloroethene

OBJECTIVES: Polychlorinated biphenyls (PCBs) and dichlorodiphenyl dichloroethene (DDE) are ubiquitous toxic environmental contaminants. Prenatal and early life exposures affect pubertal events in experimental animals. We studied whether prenatal or lactational exposures to background levels of PCBs or DDE were associated with altered pubertal growth and development in humans.Study design: Follow-up of 594 children from an existing North Carolina cohort whose prenatal and lactational exposures had previously been measured. Height, weight, and stage of pubertal development were assessed through annual mail questionnaires. RESULTS: Height of boys at puberty increased with transplacental exposure to DDE, as did weight adjusted for height; adjusted means for those with the highest exposures (maternal concentration 4+ ppm fat) were 6.3 cm taller and 6.9 kg larger than those with the lowest (0 to 1 ppm). There was no effect on the ages at which pubertal stages were attained. Lactational exposures to DDE had no apparent effects; neither did transplacental or lactational exposure to PCBs. Girls with the highest transplacental PCB exposures were heavier for their heights than other girls by 5.4 kg, but differences were significant only if the analysis was restricted to white girls. CONCLUSIONS: Prenatal exposures at background levels may affect body size at puberty.     

Prevention and treatment of overweight and obesity in children and adolescents

Increasing numbers of obese children and adolescents all over the world demand an investment in the primary and secondary prevention of obesity and overweight in this age group. The goal of preventive measures in children is to avoid the negative short- and long-term health problems associated with obesity. Primary prevention aims at establishing a healthy, active lifestyle and keeping children and adolescents within a range of body weight which is considered to be healthy. Constant availability and affordability of palatable and energy-dense food in the affluent society of the western world demands preventive strategies. Universal or public health prevention seems to be the most suitable form because several other cofactors of morbidity and mortality of affluent societies can also be prevented. However, in most European countries there is a lack of awareness of the necessity of prevention programmes, not only among the general population but also among the medical society. More awareness and consciousness to the problem of obesity must be generated in order to lead to effective therapeutic programmes. For those children and adolescents who are already obese, secondary prevention is mandatory. Therapeutic intervention programmes for the obese aim at long-term weight maintenance and normalisation of body weight and body fat. They have to modify eating and exercise behaviour of the obese child and establish new, healthier behaviour and lifestyle. Treatments programmes must include behavioural components in order to permanently change nutrition and physical exercise of the obese children and adolescents. However, long-term results of treatment programmes in European countries are scarce and the reported results, even of multidisciplinary regimens, are not impressive. CONCLUSION: In most European countries there is an urgent need not only for a growing awareness of the problem of obesity in children and adolescents but also for development of new comprehensive approaches in treating this group.