血管紧张素Ⅱ调节雄性大鼠催乳素和β-内啡肽的释放

本工作给清醒、自由活动的SD雄性大鼠第三脑室内注射血管紧张素Ⅱ,用放射免疫测定给药前后血浆催乳素(PRL)和β-内啡肽(β-EP)含量的变化,结果显示,注射ANGⅡ50和500ng,可显著升高血浆PRL和β-EP的含量。静脉注射多巴胺受体阻断剂spiroperidol后,也可显著升高血浆PRL水平,若在此基础上加脑室内注射50ng ANGⅡ,血浆PRL含量与单独静脉注射spiroperidol无显著差别。在体外,ANGⅡ作用于前叶垂体细胞后,可使其培养液中PRL和β-EP含量显著升高。用EGTA络合细胞外Ca~(2+)后,不影响10~(-8)M ANGⅡ所致的PRL升高,但部分抑制其升高β-EP的效应。10~(-8)M的ANGⅡ可使垂体细胞内Ca~(2+)浓度显著升高,但不影响其胞内cAMP的含量。     

脑室注入血管紧张素Ⅱ对大鼠组织和血浆环核苷酸及血浆血管紧张素Ⅱ水平的影响

肾素-血管紧张素系统(RAS)在血压调节和高血压发病中具有重要作用。而RAS本身也受到中枢神经系统的调制及多种体液因素的影响。研究证明脑内存在有血管紧张素Ⅱ受体(ANGⅡR)激活ANGⅡ可以引起血压升高等一系列变化。在肾性高血压大鼠我们曾观察到中枢和外周的环核苷酸浓度的     

高血压病与内皮素的临床与实验研究

内皮素(Endothelin,ET)是血管内皮细胞合成、释放的,是迄今所知体内最强、持续最久的缩血管活性多肽。大量的文献报告实验性高血压动物血浆ET水平明显增加,ET对血管平滑肌细胞有促增生、肥大效应,推测ET在高血压的发病过程中具有重要作用,但ET在高血压的发病学意义有待确定。本工作对原发性和继发性高血压患者以及大鼠腹主动脉狭窄造成的高血压模型上,观察了血浆ET水平的动态变化,以探讨ET在高血压中的发病学意义。材料和方法一、临床资料和方法: (一)病例选择:1.高血压93例,均系我院住院患者,其中(1)原发性高血压符合WHO诊断标准与分期的63例(男36例,女27例),年龄28～71(50.85)岁,内有Ⅰ期     

白细胞介素-2抑制内皮素对自发性高血压大鼠血管平滑肌细胞的增殖作用

本工作选用8—10周雄性自发性高血压大鼠(SHR)的胸主动脉平滑肌细胞进行传代培养,观察了内皮素(ET)对VSMC增殖的促进作用及其白细胞介素-2(IL-2)对此效应的抑制。实验分为对照组(生理盐     

原发性高血压进程中下丘脑内神经元型一氧化氮合酶和血管紧张素Ⅱ1型受体的共表达

目的:观察Wistar-Kyoto(WKY)大鼠和自发性高血压大鼠(SHR)下丘脑室旁核(PVN)和视上核(SON)内神经元型一氧化氮合酶(nNOS)和血管紧张素Ⅱ1型受体(AT-1R)的共表达,以及加压素(AVP)和nNOS基因水平的表达差异.方法:应用免疫荧光双标染色结合RT-PCR技术.结果:SHR和WKY大鼠PVN和SON内都有大量的nNOS和AT-1R免疫阳性神经元分布并部分共存,但SHR组nNOS和AT-1R共存率明显高于对照组.与之一致,SHR组PVN和SON内nNOS和AVP mRNA含量都高于对照组.结论:在高血压发病进程中,NO发生代偿性增加,可部分负反馈抑制中枢肾素-血管紧张素系统,但这种抑制不能完全逆转过度激活的血管紧张素Ⅱ和AVP.     

尾加压素Ⅱ抑制大鼠心肌细胞L型钙电流

尾加压素Ⅱ(urotensinⅡ,UⅡ)是目前发现的哺乳动物体内最强的缩血管物质,其缩血管效应比内皮素-1强10余倍[1].它具有收缩血管、促心肌细胞肥大和血管细胞增殖、抑制心功能等生物学效应,在高血压、动脉粥样硬化、心血管重塑、心力衰竭等多种心血管疾病的发生发展中可能具有重要意义.     

血管内皮素和血管紧张素Ⅱ释放的相互关系

为探讨血管内皮素(ET)和血管紧张素Ⅱ(AⅡ)释放的相互关系,本工作用放射免疫方法测定离体灌流大鼠主动脉的ET和AⅡ的释放,发现EF或AⅡ呈剂量依赖地促进主动脉条释放AⅡ或EF。缺氧可显著地促进ET和AⅡ的释放,而ET或AⅡ抗血清明显地抑制缺氧所致的AⅡ或ET的释放。临床观察发现血管紧张素转换酶抑制剂—巯甲丙脯酸治疗原发性高血压,有效地降低病人血浆ET水平。结果提示:血管AⅡ和ET的释放间存在着相互促进的正反馈关系。     

血管紧张素Ⅱ在自发性高血压大鼠主动脉重建中的作用

目的:探讨血管紧张素Ⅱ(AngⅡ)在高血压主动脉重建中的作用。方法:选用AngⅡ受体I亚型拮抗剂losartan,对雄性自发性高血压大鼠(SHR)进行为期10周的治疗,观察并比较其在剂量15 mg/kg·d^-1及0.75 mg/kg·d-1时,对16周到26周SHR胸主动脉重建的影响。结果:Losartan 15 mg在降低血压的同时, 通过抑制主动脉中膜平滑肌细胞(VSMC)的肥大明显抑制了主动脉肥厚,losartan 0.75 mg未能使血压下降的情况下,对VSMC及主动脉肥厚均没有影响。Losartan对胶原纤维的作用与对VSMC的作用不同,两种剂量的losartan均明显抑制了胶原纤维的合成。结论:AngⅡ对SHR主动脉平滑肌生长的调节可能为压力依赖性,对胶原纤维的作用则可能是通过非压力机制。     

胰岛素对高血压大鼠血管平滑肌细胞血小板源生长因子A链和转化生长因子β_1表达的影响

探讨胰岛素对体外培养的血管平滑肌细胞 (VSMC)增生及其长型血小板源生长因子A (PDGF A)链和转化生长因子 β1(TGFβ1)mRNA表达的影响。结果发现 :(1)胰岛素促进自发型高血压大鼠的血管平滑肌细胞(SHR -VSMC)增生 ,且呈浓度依赖性 ;而对正常血压的Wistar kyota大鼠的血管平滑肌细胞 (WKY -VSMC)增生无影响。 (2 )定量RT -PCR分析显示 ,胰岛素加强WKY -VSMC的TGFβ1mRNA的表达 (P <0 0 1) ,但是减少SHR -VSMC的TGFβ1mRNA的表达 (P <0 0 0 1)。 (3)胰岛素对二株系VSMC的长型PDGF A链相对表达水平无影响。结果表明 ,胰岛素选择性地加强SHR -VSMC的增殖 ,而对WKY -VSMC的增殖无影响 ,这可能和胰岛素能上调WKY -VSMC自分泌TGFβ1有关 ;而在SHR -VSMC ,此反馈抑制失常 ,结果SHR -VSMC加速生长。     

伴有高血压的糖尿病大鼠主动脉的结构重建

目的 :观察伴有高血压的糖尿病 (SHRDM)主动脉结构重建的规律 ,并探讨高血糖、高血压对其影响。方法 :STZ诱导SHR大鼠建立SHRDM实验动物模型 ,。观测主动脉血管壁中膜结构成分的改变。结果 :SDDM(有高血压的糖尿病 )大鼠自 4周始主动脉中膜平滑肌相对含量和核密度、胶原纤维相对含量均大于SD组 ,弹性纤维相对含量少于SD组。SHRDM组主动脉平滑肌相对面积、C/E值大于SD和SHR组 ,但SMC核数少于SDDM ,多于SHR。结论 :糖尿病早期已出现主动脉结构重建 ,以平滑肌增生为主 ;高血压使平滑肌细胞肥大为主 ,因而SHRDM增生、肥大共存。高血压、高血糖均显著影响主动脉结构重建 ,高血压影响大于高血糖。     

Level of functioning of siblings and parents of probands of varying degrees of retardation

A further analysis of already published data supports the position that retardates of low ability level less frequently have retarded siblings, retarded parents, and parents low in occupational level than do retardates higher in ability level. The analysis supports the position that there are two types of retarded individuals, persons retarded as a result of gene or chromosomal anomalies, brain injury, etc., who more frequently occur in the lower-level retardate group, and persons whose retardation represents polygenic segregation, who more frequently occur in the higher-level group.     

Modes of Inheritance of Errors of Refraction

Eighteen families in which both parents had refractions within the range of +4·0 D to −4·0 D and axial lengths seen in emmetropia (22·3-26·0 mm) showed coefficients of correlation of the order 0·5 indicative of polygenic inheritance. Such coefficients were seen for axial length (0·407) and for the cornea (0·487), but not for the lens (which is known to be yoked to the axial length). No such coefficients were seen in 19 families in which one of the parents had axial length outside the emmetropic range (nine families with long axes and 10 with short axes).

The pattern of polygenic inheritance for emmetropia (completely correlated optical components) and errors of refraction up to 4·0 D (inadequately correlated components: correlation ametropia) follows that seen in stature and other measurable characters. In contrast the high refractive errors with their abnormal axial lengths (component ametropia) are—like the extremes in stature—pathological anomalies with monofactorial inheritance.

     

Aspects of the problem of direct introduction of Standards of International Organizations

Editorial note. This article is published as part of a discussion. Particular issues of the article are disputable. First of all, this concerns the so-called “folder” method of introduction of international standards for medical devices to domestic medical practice (i.e., by direct translation of the standards and their publication as standardizing documents). Nevertheless, at least one of the problems, the problem of coordination between domestic state standards for medical devices and international recommendations of ISO and IEC, is undoubtedly of topical importance. Advancement of new health service legislation which is to be approved by law-makers will definitely introduce corrections into the present situation. The Editorial Board of Meditsinskaya Tekhnika believes this article will lessen these problems and to be welcomed by readers.