络活喜对自发性高血压大鼠血管壁重塑的实验研究

目的探讨络活喜(amlodipine)对自发性高血压大鼠(spontaneously hypertensive rats,SHR)血管壁重塑生物学机制。方法将10周龄雄性24只SHR随机分成3组,每组8只。对照组(SHRC)不作治疗,并与同周龄Wistar鼠组(n=8)作比较。生理盐水组(SHRNS),络活喜组(SHRA)分别经生理盐水、络活喜治疗8周后光镜观察血管几何形态,采用原位杂交及半定量RT-PCR方法检测ET-1(endothelin-1)、MMP-2(matrix metal-loproteinase-2)表达水平。结果对照组,生理盐水组血压明显增高,管腔增大,管壁明显增厚(P<0.05),尤以血管中层平滑肌细胞(vascular smooth cell,VSMC)肥大为主(P<0.01);ET-1,MMP-2表达显著增加(P<0.05)。治疗8周后,络活喜组血压明显降低,管壁变薄;ET-1、MMP-2表达减少(P<0.05)。结论络活喜可能通过抑制血管壁ET-1与MMP-2表达,遏制自发性高血压大鼠血管壁重塑。     

络丁新络活喜对原发性高血压左室肥厚的影响

目的　观察络丁新络活喜降压疗效及对原发性高血压 (EH)左室肥厚 (LVH )的影响。方法　将 85例EH并LVH随机分为两组 ,分别给予络丁新 (剂量 10mg ,qd或Bid) ,络活喜 (剂量 5mg ,qd或Bid) ,疗程 1年 ,于服药前和服药后 6、12个月测血压 ,同时用超声心动图观察左心室舒张末期内径 (LVDd) ,心室间隔舒张末期厚度 (IVST) ,左心室后壁舒张末期厚度 (PWT)及左心室重量指数 (LVMI)。结果　两种药均能有效降低EH患者收缩压及舒张压 (P <0 0 1) ,明显改善LVDd ,IVST ,PWT(P <0 0 1) ,LVMI(P <0 0 0 1)。结论　络丁新络活喜能有效控制血压 ,且对EH的LVH有逆转作用     

络活喜治疗老年原发性高血压的临床观察

络活喜治疗老年原发性高血压的临床观察江苏省老年医院内科（２１００２４）季宏老年原发性高血压病发病率高，合并症多，且老年人自身调节机能的减弱，药物副反应大，加之服用降压药是一个长期过程，故降压药选择尤为重要。笔者应用新一代钙拮抗剂络活喜（苯磺酸氨氯地平...     

安博维合用络活喜对原发性高血压病的疗效

血管紧张素转换酶抑制剂（ACEI）福辛普利和络活喜合用是常见的较好的降压方案。本文将血管紧张素Ⅱ（AngⅡ）受体阻滞剂（ARB）安博维和络活喜合用与其比较，观察在降压的疗效上两者有无明显差异。结果如下。     

依伦平与络活喜治疗高血压的疗效比较

目的 比较依伦平与络活喜治疗原发性高血压的降压疗效及安全性.方法 选择100例原发性高血压患者,随机分为依伦平组(50例),络活喜组(50例),两种药物均为口服片剂,每天一片晨服,连续观察四周,每周一上午测血压、心率和不良反应.用药前和用药后4周末检测血液生化指标.结果 两组病例服药2周后收缩压、舒张压均下降,服药4周后收缩压、舒张压均显著下降,不良反应率分别为10%和12%,差异无显著性.结论 依伦平和络活喜均能达到很好的降压疗效,安全性好,不良反应率低.     

络活喜和雅施达对高血压患者血压昼夜节律的影响研究

目的观察络活喜与雅施达对高血压昼夜节律的影响。方法使用动态血压监测选出非杓式高血压患者251例,将患者随机分为络活喜组和雅施达组,用药8周后,重复动态血压监测比较二者对高血压患者血压昼夜节律影响。结果二者在降压方面无显著性差异,络活喜组有33例恢复杓型血压,雅施达组有51例恢复杓型血压,差异有统计学意义。结论雅施达能更好的逆转非杓式高血压的昼夜节律。     

搏苏与络活喜治疗高血压效果的比较

目的：探讨博苏与络活喜对高血压病的疗效。方法：40例高血压病人随机被分为两组,分别服用博苏与络活喜,4周后评定疗效。结果：两组病人的血压在治疗后均有显下降（P＜0．001）。结论：博苏与络活喜治疗高血压均有降压效果稳定、确切、持久的作用,而且副作用小。     

血清一氧化氮在动脉粥样硬化性疾病患者中的变化

目的　探讨血清一氧化氮 (NO)含量在动脉粥样硬化性疾病患者中的变化及其在动脉粥样硬化性疾病发病机制中的可能作用。方法　应用比色法 ,测定 66例健康体检者、63例动脉粥样硬化性疾病患者血清NO水平。结果　疾病组血清NO均显著低于对照组 (均P <0 0 1)。结论　NO在动脉粥样硬化性疾病的病理生理改变中起重要作用     

络活喜与安博维联合治疗老年性高血压疗效观察

本科从2004年至2007年收治的老年中度高血压患者,联用络活喜与安博维观察降压疗效及其左室舒张功能,现报告如下：     

血清一氧化氮在动脉粥样硬化性疾病患者中的变化

目的探讨血清一氧化氮(NO)含量在动脉粥样硬化性疾病患者中的变化及其在动脉粥样硬化性疾病发病机制中的可能作用.方法应用比色法,测定66例健康体检者、63例动脉粥样硬化性疾病患者血清NO水平.结果疾病组血清NO均显著低于对照组(均P<0.01).结论 NO在动脉粥样硬化性疾病的病理生理改变中起重要作用.     

糖尿病大鼠一氧化氮与骨代谢变化的研究

目的　研究糖尿病 (DM )大鼠血清一氧化氮 (NO)与早期骨代谢改变的关系。方法2 0只SD大鼠分为 2组 ,一组以链脲佐菌素诱导建立糖尿病 (STZ DM )大鼠模型 ,另一为正常对照组 ,测定 2组大鼠的空腹血糖 (FBG)、HbA1c、血清胰岛素、全身、股骨和腰椎骨密度 (BMD)、骨代谢相关指标〔血清钙、骨钙素、降钙素、甲状旁腺素 (PTH)、维生素D3 及尿吡啶酚 /肌酐比〕和血清NO水平。结果　STZ DM大鼠与正常对照组相比 ,血清NO水平显著升高〔(5 1.3± 11.9vs 38.1± 12 .0 )μmol/L ,P <0 .0 1〕 ;全身、股骨和腰椎的BMD显著降低〔(0 .15± 0 .0 7vs 0 .2 1± 0 .0 2 ) g/cm2 ,P<0 .0 1;(0 .16± 0 .0 2vs 0 .19± 0 .0 3) g/cm2 ,P <0 .0 5 ;(0 .12± 0 .0 4vs 0 .18± 0 .0 6 ) g/cm2 ,P <0 .0 5〕 ;血清钙浓度显著升高〔(135 .9± 11.3vs 117.2± 6 .5 )mg/L ,P <0 .0 0 1〕 ,骨钙素水平显著升高〔(0 .0 7± 0 .0 4vs 0 .0 5± 0 .0 1) μg/L ,P <0 .0 5〕 ,维生素D3 水平显著降低〔(7.6± 1.9vs 11.6± 4 .1)μg/L ,P <0 .0 5〕 ,尿吡啶酚 /肌酐显著降低〔(4.8± 0 .8vs 75 .8± 6 0 .7)nmol/mmolCr,P <0 .0 1〕 ;而降钙素和PTH水平改变无统计学意义。相关性分析显示 ,血清NO与尿吡啶酚排泄呈负相关 (r= - 0 .74 ,     

西藏大骨节病患者血清透明质酸、一氧化氮和硒水平检测分析

目的测定西藏成人大骨节病患者血清透明质酸(HA)、一氧化氮(NO)和硒(Se)水平的变化,探讨HA、NO和Se在西藏大骨节病发生发展的机理。方法在西藏拉萨大骨节病病区随机选取大骨节病患者30例(大骨节病组)、病区内健康者30例(病区内对照组)、非大骨节病病区健康者30例(病区外对照组),3组人群年龄、性别无显著差异。采取静脉血离心制备血清,用酶联免疫吸附试验(ELISA)检测HA、硝酸还原酶法测定NO、荧光法测定血清Se水平。结果①大骨节病组、病区内、外对照组血清HA水平分别为(68．56±8．34)、(90．55±18．25)、(92．18±14．61)μg/L,大骨节病组血清HA水平显著低于病区内、外健康对照组(P<0．05);②3组血清NO水平分别为(102．98±26．15)、(35．73±13．32)、(34．65±12．21)μmol／L,大骨节病组血清NO水平显著高于病区内、外健康对照组(P<0．05);③3组血清Se水平分别为(73．34±22．72)、(68．76±20．56)、(98．73±37．20)μg／L,病区人群血清Se水平显著高于非病区人群(P<0．05);④血清HA水平与血清Se水平呈显著正相关(r=0．196,P<0．05),血清Se水平与NO水平有负相关趋势,但差异无统计学意义(r=～0．085,P>0．05)。结论西藏成人大骨节病的发生发展与血清HA水平降低和NO水平升高有关。     

大鼠同种异位心脏移植术后血清NO及心肌组织NOS活性的观察

目的　研究内源性一氧化氮（ＮＯ）与心脏移植急性排斥反应的关系。方法　本研究以大鼠同种异位心脏移植为研究对象,观察了术后３、５、７ 天的血清ＮＯ 水平以及心肌组织一氧化氮合成酶（ＮＯＳ）的活性。结果　在急性排斥反应发生的早期开始血清ＮＯ 水平就已显著升高（术后３、５、７ 天皆为Ｐ ＜ ０．０１）;心肌组织ＮＯＳ活性亦显著高于对照组（术后３ 天Ｐ ＜ ０．０５,术后５ 天Ｐ＜ ０．０１,术后７ 天Ｐ ＜ ０．０５）。结论　血清ＮＯ 水平的检测对于心脏移植急性排斥反应的发生可能具有早期的辅助诊断意义。     

促红素对肝硬化大鼠血清—氧化氮含量的影响

目的探讨血红蛋白（Ｈｂ）对肝硬化大鼠血清一氧化氮（ＮＯ）含量及血流动力学的影响。方法应用５７Ｃｏ标记微球观察促红素长期治疗对肝硬化大鼠血流动力学参数的影响；应用荧光法测定大鼠血清ＮＯ含量。结果肝硬化大鼠全部出现高动力循环状态，且血清ＮＯ含量显著高于对照组、血Ｈｂ含量显著低于对照组；促红素治疗组，高动力循环状态明显改善，与未治疗组比较，Ｈｂ含量显著升高，血清ＮＯ含量显著降低。结论促红素致Ｈｂ增加，进而加速ＮＯ灭活对肝硬化高动力循环状态可能具有潜在治疗作用     

Hypothyroidism: age-related influence on cardiovascular nitric oxide system in rats

This study investigates whether changes in nitric oxide (NO) production participate in the cardiovascular manifestations of hypothyroidism and whether these changes are age-related. Sprague-Dawley rats aged 2 and 18 months old were treated with 0.02% methimazole (wt/vol) during 28 days. Left ventricular function was evaluated by echocardiography. Measurements of arterial blood pressure, heart rate, nitric oxide synthase (NOS) activity and NOS/caveolin-1 and -3 protein levels were performed. Hypothyroidism enhanced the age-related changes in heart function. Hypothyroid state decreased atrial NOS activity in both young and adult rats, associated with a reduction in protein levels of the three NOS isoforms in young animals and increased caveolin (cav) 1 expression in adult rats. Ventricle and aorta NOS activity increased in young and adult hypothyroid animals. In ventricle, changes in NOS activity were accompanied by an increase in inducible NOS isoform in young rats and by an increase in caveolins expression in adult rats. Greater aorta NOS activity level in young and in adult Hypo rats would derive from the inducible and the endothelial NOS isoform, respectively. Thyroid hormones would be one of the factors involved in the modulation of cardiovascular NO production and caveolin-1 and -3 tissue-specific abundance, regardless of age. Hypothyroidism appears to contribute in a differential way to aging-induced changes in the myocardium and aorta tissues. Low thyroid hormones levels would enhance the aging effect on the heart. Age-related changes in NO production participate in the cardiovascular manifestations of hypothyroidism.     

硝酸甘油治疗大鼠骨质疏松症血清NO、NOS的变化

目的初步探讨用硝酸甘油治疗骨质疏松症(OP)及其与一氧化氮(NO)、一氧化氮合酶(NOS)的关系。方法将40只6月龄雌性大鼠随机分成假手术组(15只)和OP模型组(25只),其中OP模型组去卵巢造成骨质疏松模型,从其中随机选5只大鼠测定血清NO、NOS的变化,并与5只假手术组大鼠比较。剩余OP模型组大鼠随机分为OP对照组(10只)与硝酸甘油治疗组(10只),硝酸甘油治疗组经硝酸甘油治疗骨密度升高后,测其血清NO、NOS的变化,并与OP对照组及假手术组比较。结果OP模型组血清NO、NOS低于假手术组(P<0.01,P<0.05)。硝酸甘油治疗组大鼠骨密度升高后,其血清NO、NOS高于OP对照组(P<0.01,P<0.05),而与假手术组差异无显著意义(P>0.05)。结论NO、NOS参与了骨质疏松症的病理生理过程,硝酸甘油治疗骨质疏松症可能与NO、NOS有关。     

Reduced influence of nitric oxide on arteriolar tone in hypertensive Dahl rats.

The aim of this study was to evaluate the influence of endogenous nitric oxide on resting microvascular tone in the Dahl salt-sensitive (DS) rat and to determine how this influence is altered in salt-induced hypertension. Intravital microscopy was used to examine the arteriolar network in the spinotrapezius muscle of DS rats maintained on low (0.45% NaCl) or high (4% NaCl) salt diets for 6-7 weeks. Mean arterial pressure for DS rats on high salt (163 +/- 3 mm Hg) was significantly greater than that for DS rats on low salt (128 +/- 4 mm Hg). Inhibition of microvascular nitric oxide synthesis with NG-nitro-L-arginine-methyl ester caused arteriolar constriction in normotensive DS but not in hypertensive DS rats. Application of L-arginine consistently caused arteriolar dilation in normotensive DS but not hypertensive DS rats. In contrast, arteriolar responses to iontophoretically applied acetylcholine and sodium nitroprusside were similar in both groups. These results indicate that basal release of nitric oxide, presumably from the endothelium, normally influences arteriolar tone in skeletal muscle of DS rats and that this influence is suppressed in established salt-induced hypertension. However, the normal arteriolar response to acetylcholine in hypertensive DS rats suggests that a generalized impairment of endothelial function may not occur in the microcirculation of these animals. Unaltered arteriolar responsiveness to sodium nitroprusside in hypertensive DS rats also suggests that salt-induced hypertension is not accompanied by a change in the responsiveness of arteriolar smooth muscle to nitric oxide.     

The influence of endothelium-derived nitric oxide on myocardial contractile function

Nitric oxide released by cardiac endothelial cells modulates myocardial contractile function through elevation of intracellular 3′,5′-cyclic guanosine monophosphate (cGMP). In the absence of agonist stimulation, nitric oxide typically enhances myocardial relaxation and reduces diastolic tone, without significantly altering the rate of force or pressure development. This pattern of effect is observed with nitric oxide or with cGMP analogues in isolated rat cardiac myocytes, isolated ferret papillary muscle preparations, and isolated ejecting guinea-pig hearts. In human subjects studied at cardiac catheterisation, low-dose bicoronary infusions of sodium nitroprusside or of substance P induce similar effects on left ventricular systolic and diastolic function. These changes may benefit from cardiac filling and coronary perfusion by increasing the diastolic interval, reducing extravascular compressive forces and increasing the driving pressure for filling, e.g., during exercise. Nitric oxide may also modulate inotropic and chronotropic responses to β-adrenergic stimulation. Under pathological conditions, overproduction of nitric oxide by an inducible nitric oxide synthase may be detrimental for contractile function. Dysfunction of the constitutive nitric oxide pathway could also contribute to pathophysiology, e.g., in conditions characterised by diastolic dysfunction. The paracrine nitric oxide pathway is likely to be an important regulator of cardiac contractile function, acting in concert and interacting with other regulatory pathways.     

自发性高血压大鼠血清和心肌一氧化氮浓度的变化及L-精氨酸对其抑制作用

目的 :观察补充左旋精氨酸 4周后 12～ 13周龄自发性高血压大鼠 (SHR)血清和心肌组织一氧化氮(NO)浓度及血压的变化。方法 :通过腹腔注射补充NO合成前体———左旋精氨酸 (L Arg) 4周 ,硝酸还原酶法测定血清和心肌组织NO浓度 ;鼠尾压测量仪测量大鼠尾动脉的收缩压。结果 :治疗组SHR与对照组SHR相比心肌NO浓度降低 (P <0 .0 5 ) ,两组间血清NO浓度、血压差异无显著性意义 (P >0 .0 5 )。结论 :SHR 12～ 13周龄时体内NO呈代偿性地升高 ,通过腹腔注射慢性补充L Arg 4周使心肌组织NO浓度下降 ,但未能降低SHR已形成的高血压。     

动脉瘤性蛛网膜下腔出血患者血液及脑脊液中内皮素和一氧化氮含量变化

目的探讨动脉瘤性蛛网膜下腔出血（ＳＡＨ）患者血液及脑脊液中内皮素（ＥＴ）和一氧化氮（ＮＯ）的含量与脑血管痉挛（ＣＶＳ）及临床病情的关系。方法采用放射免疫方法测定血液和脑脊液中ＥＴ含量;采用硝酸还原酶法测定血液和脑脊液中ＮＯ的代谢产物ＮＯ－ｘ（ＮＯ－２和ＮＯ－３）含量。结果ＳＡＨ后血液和脑脊液中ＥＴ含量增高（Ｐ＜００５）,且重症组高于轻症组（Ｐ＜００５）;而ＳＡＨ后血液和脑脊液中ＮＯ含量则下降（Ｐ＜００５）,重症组下降更加明显（Ｐ＜００５）。结论提示ＳＡＨ后脑血管痉挛和迟发性脑缺血可能系ＥＴ升高和ＮＯ下降使大脑动脉持续收缩所致,且临床症状的严重程度与ＥＴ增高和ＮＯ下降的程度密切相关。本实验结果支持ＳＡＨ后ＣＶＳ发生机制中ＥＴ与ＮＯ动态平衡破坏学说。