BACKGROUND & AIMS: BACKGROUND:The ELITE study showed an association between the angiotensin II antagonist losartan and an unexpected survival benefit in elderly heart-failure patients, compared with captopril, an angiotensin-converting-enzyme (ACE) inhibitor. We did the ELITE II Losartan Heart Failure Survival Study to confirm whether losartan is superior to captopril in improving survival and is better tolerated. METHODS:We undertook a double-blind, randomised, controlled trial of 3,152 patients aged 60 years or older with New York Heart Association class II-IV heart failure and ejection fraction of 40% or less. Patients, stratified for beta-blocker use, were randomly assigned losartan (n=1,578) titrated to 50 mg once daily or captopril (n=1,574) titrated to 50 mg three times daily. The primary and secondary endpoints were all-cause mortality, and sudden death or resuscitated arrest. We assessed safety and tolerability. Analysis was by intention to treat. FINDINGS:Median follow-up was 555 days. There were no significant differences in all-cause mortality (11.7 vs 10.4% average annual mortality rate) or sudden death or resuscitated arrests (9.0 vs 7.3%) between the two treatment groups (hazard ratios 1.13 [95.7% CI 0.95-1.35], p=0.16 and 1.25 [95% CI 0.98-1.60], p=0.08). Significantly fewer patients in the losartan group (excluding those who died) discontinued study treatment because of adverse effects (9.7 vs 14.7%, p<0.001), including cough (0.3 vs 2.7%).

背景与目标： 背景：ELITE研究表明，与血管紧张素转换酶（ACE）抑制剂卡托普利相比，血管紧张素II拮抗剂洛沙坦与老年心衰患者的意外生存获益之间存在关联。我们进行了ELITE II Losartan心力衰竭生存研究，以确认氯沙坦在改善生存率和耐受性方面是否优于卡托普利。
方法：我们进行了一项双盲，随机，对照试验，研究对象为3,152名60岁以上的纽约心脏协会II-IV级心力衰竭且射血分数小于或等于40％的患者。随机分组接受β-受体阻滞剂治疗的患者，每天随机分配一次洛沙坦（n = 1,578）滴定至50 mg或每天3次将卡托普利（n = 1,574）滴定至50 mg。主要终点和次要终点是全因死亡率，突然死亡或复苏的逮捕。我们评估了安全性和耐受性。分析是按意向进行的。
结果：中位随访时间为555天。两个治疗组之间的全因死亡率（年平均死亡率分别为11.7和10.4％）或突然死亡或复苏的逮捕（9.0和7.3％）没有显着差异（危险比1.13 [95.7％CI 0.95-1.35]， p = 0.16和1.25 [95％CI 0.98-1.60]，p = 0.08）。氯沙坦组中，因不良反应（9.7 vs 14.7％，p <0.001），包括咳嗽（0.3 vs 2.7％）而中止研究治疗的患者显着减少（不包括死亡的患者）。

BACKGROUND & AIMS: :Lipid peroxides and fluorescent serum proteins, possible markers of free radical activity, are increased in diabetic patients, particularly those with angiopathy. Captopril, an angiotensin converting enzyme (ACE) inhibitor, scavenges free radicals in vitro independently of ACE inhibition. This is probably due to the presence of a sulphydryl group which is not present in other ACE inhibitor drugs. We have compared the effects of captopril and enalapril on free radical activity in thirty-two diabetic subjects with hypertension (BP greater than 160/95 mmHg). After a three week run-in period on no antihypertensive therapy, patients were randomly allocated to receive captopril or enalapril, the dose titrated according to BP response. After three months, BP was well controlled in both groups and glycaemic control unchanged. Both drugs were associated with a reduction of fluorescent IgG (captopril:Baseline [BL] 0.564 vs. 12 weeks [w] 0.428, P less than 0.05, enalapril:BL 0.603 vs. 12w 0.422 P less than 0.05) and thiobarbituric acid reactive material (captopril:BL 2.35 nmol MDA vs. 12w 1.46 nmol, P less than 0.05, enalapril:BL 2.44 nmol vs. 12w 1.72 nmol, P less than 0.01). In contrast to in vitro studies, there was no significant difference between the drugs when used in therapeutic doses, questioning a hypothesised advantage of captopril over enalapril.

背景与目标： ：脂质过氧化物和荧光血清蛋白，可能是自由基活性的标志物，在糖尿病患者，特别是患有血管病的患者中增加。卡托普利是一种血管紧张素转化酶（ACE）抑制剂，可在体外独立于ACE抑制清除自由基。这可能是由于存在其他ACE抑制剂药物中不存在的巯基。我们比较了卡托普利和依那普利对32例糖尿病高血压患者的自由基活性的影响（血压大于160/95 mmHg）。经过三周的无高血压治疗磨合期后，患者被随机分配接受卡托普利或依那普利治疗，剂量根据BP反应而调整。三个月后，两组血压均得到良好控制，血糖控制未改变。两种药物均与荧光IgG（卡托普利：基线[BL] 0.564比12周[w] 0.428，P小于0.05，依那普利：BL 0.603与12w 0.422 P小于0.05）的降低和硫代巴比妥酸反应性物质有关。 （卡托普利：BL 2.35 nmol MDA相对于12w 1.46 nmol，P小于0.05，依那普利：BL 2.44 nmol对12w 1.72 nmol，P小于0.01）。与体外研究相反，当以治疗剂量使用时，两种药物之间没有显着差异，这质疑了卡托普利相对于依那普利的假设优势。

BACKGROUND & AIMS: :The purpose of current study was to examine the possible involvement of captopril, an angiotensin-converting enzyme inhibitor, on nociception, morphine analgesia and morphine tolerance development involving inflammation and ER-stress pathways in rats. In this study, thirty-six male Wistar rats were used. Animals were divided into six groups: Saline, 50 mg/kg captopril, 5 mg/kg morphine, morphine + captopril, morphine tolerance and morphine tolerance + captopril. The resulting analgesic effect was measured with hot plate and tail flick analgesia tests. The dorsal root ganglions (DRG) tissues were collected for inflammation parameters, endoplasmic reticulum (ER) stress and apoptosis proteins by using ELISA. Captopril showed anti-nociceptive effect when given alone (p < 0.05 to p < 0.01). In addition, captopril increased the analgesic effect of morphine (p < 0.05 to p < 0.001) and also decreased the tolerance to morphine at a significant level (p < 0.05 to p < 0.001). However, it decreased inflammation and ER-stress when applied with single-dose morphine and tolerance induction (p < 0.001). Moreover, captopril decreased apoptosis proteins after tolerance development (p < 0.001). In conclusion, captopril has antinociceptive properties, increasing analgesic effect of morphine, and preventing tolerance development. These effects may occur by suppressing inflammation and ER-stress pathways.

背景与目标： ：本研究的目的是研究血管紧张素转化酶抑制剂卡托普利对涉及炎症和内质网应激通路的伤害感受，吗啡镇痛和吗啡耐受性发展的可能影响。在这项研究中，使用了三十六只雄性Wistar大鼠。将动物分为六组：盐水，50mg / kg卡托普利，5mg / kg吗啡，吗啡卡托普利，吗啡耐受性和吗啡耐受性卡托普利。通过热板和甩尾镇痛测试来测量所产生的镇痛效果。使用ELISA收集背根神经节（DRG）组织的炎症参数，内质网（ER）应激和凋亡蛋白。卡托普利单独使用时显示抗伤害作用（p <0.05至p <0.01）。此外，卡托普利提高了吗啡的镇痛作用（p <0.05至p <0.001），并且在一定水平上也降低了对吗啡的耐受性（p <0.05至p <0.001）。但是，与单剂量吗啡和耐受性诱导剂一起使用时，它可以减少炎症和内质网应激（p <0.001）。此外，卡托普利在耐受性发展后降低凋亡蛋白（p <0.001）。总之，卡托普利具有镇痛作用，可增强吗啡的止痛作用，并防止耐受性的发展。这些作用可能是通过抑制炎症和内质网应激途径而发生的。

BACKGROUND & AIMS: Congestive heart failure (CHF) is a syndrome characterized by increased levels of angiotensin II (Ang II) and endothelin-1 (ET-1). In vitro, Ang II stimulates ET-1 release. The purpose of the study was to assess the effect of a single dose of an angiotensin-converting enzyme inhibitor (ACEI) captopril versus placebo on plasma endothelin concentration in human congestive heart failure. Captopril (25 mg, given orally) was compared with placebo in a group of 20 patients with systolic dysfunction in a double-blind randomized study. Plasma irET concentration was significantly increased in CHF patients compared with normal subjects (5.59 pg/ml +/- 0.35 vs. 3.58 pg/ml +/- 0.99, p < 0.0002). Despite the decrease in systolic blood pressure and the increase in plasma renin activity, suggesting a significant blockade of the renin-angiotensin system, no difference in plasma irET-1 was observed between captopril and placebo. Our results suggest that captopril does not acutely influence irET-1 plasma concentration in human CHF. These data do not support the hypothesis that the acute vasodilator effect of a single dose of 25 mg of captopril given daily orally involves modulation of the increased plasma concentration of endothelin observed in CHF.

背景与目标： 充血性心力衰竭（CHF）是一种以血管紧张素II（Ang II）和内皮素1（ET-1）水平升高为特征的综合征。在体外，Ang II刺激ET-1释放。该研究的目的是评估单剂量血管紧张素转换酶抑制剂（ACEI）卡托普利与安慰剂对人充血性心力衰竭血浆内皮素浓度的影响。在一项双盲随机研究中，将卡托普利（25毫克，口服）与20例收缩期功能障碍的患者的安慰剂进行了比较。与正常受试者相比，CHF患者的血浆irET浓度显着增加（5.59 pg / ml /-0.35和3.58 pg / ml /-0.99，p <0.0002）。尽管收缩压降低和血浆肾素活性增加，提示肾素-血管紧张素系统被显着阻断，但卡托普利和安慰剂之间的血浆irET-1没有差异。我们的结果表明，卡托普利不会严重影响人CHF中的irET-1血浆浓度。这些数据不支持这样的假说，即每天口服25 mg卡托普利的单次剂量的急性血管扩张作用涉及调节CHF中所观察到的内皮素血浆浓度的升高。

BACKGROUND & AIMS: :Three groups of New Zealand white rabbits were used to study the effects of captopril on the renin-angiotensin system and sympathetic nervous system during sodium nitroprusside (SNP)-induced hypotension and halothane anesthesia. Two groups of rabbits (C and CH) were treated with captopril 2 mg/kg i.v. One captopril-treated group (CH) and the third, untreated group (H) received SNP to induce hypotension. In these two groups, the mean arterial blood pressure (MAP) was reduced by 40% for 150 min. Group C did not undergo SNP-induced hypotension and served to document the effects of captopril alone during the 150-min study period. Arterial blood samples for norepinephrine (NE), epinephrine (EPI), and plasma renin activity (PRA) were drawn prior to, during hypotension, and in the recovery period. The SNP dose required to maintain the hypotension was continuously recorded. NE, EPI, and PRA all increased in group H, indicating activation of both the renin-angiotensin system and the sympathetic system during hypotension. This was accompanied by a dramatic increase in SNP dose requirement. In the CH group, PRA levels rose sharply and remained elevated. Plasma NE levels increased, while EPI levels remained unchanged with a decline in the SNP dose requirement. The C group demonstrated a rise in PRA levels, accompanied by unchanged NE and EPI levels and MAP during the study period. Captopril administration decreased the SNP dose requirement and significantly decreased the sympathetic response (measured by NE and EPI levels) in group CH as compared to the H group.(ABSTRACT TRUNCATED AT 250 WORDS)

背景与目标： ：三组新西兰白兔用于研究卡托普利对硝普钠（SNP）引起的低血压和氟烷麻醉下肾素-血管紧张素系统和交感神经系统的影响。两组兔子（C和CH）分别经卡托普利2 mg / kg静脉内治疗。一个卡托普利治疗组（CH）和第三个未经治疗组（H）接受SNP诱导低血压。在这两组中，平均动脉压（MAP）在150分钟内降低了40％。 C组未经历SNP引起的低血压，并在150分钟的研究期内用于证明卡托普利的作用。在降压之前，降压期间和恢复期间抽取了去甲肾上腺素（NE），肾上腺素（EPI）和血浆肾素活性（PRA）的动脉血样品。持续记录维持低血压所需的SNP剂量。 H组的NE，EPI和PRA均升高，表明低血压期间肾素-血管紧张素系统和交感神经系统均被激活。这伴随着SNP剂量需求的急剧增加。在CH组，PRA水平急剧上升并保持较高水平。血浆NE水平增加，而EPI水平保持不变，但SNP剂量要求却下降了。在研究期间，C组表现出PRA水平升高，同时NE和EPI水平和MAP保持不变。与H组相比，卡托普利给药降低了CH组的SNP剂量需求并显着降低了交感反应（通过NE和EPI水平测量）（摘要截断为250字）

BACKGROUND & AIMS: :To study the hemodynamic and neurohumoral effects of hydralazine versus captopril after the first dose, 15 patients with idiopathic dilated cardiomyopathy (NYHA Class II and III) were included in a crossover trial with a washout period of three days. Hemodynamic parameters were measured by using a Swan-Ganz thermodilution catheter, and venous blood was sampled during supine rest and standardized upright exercise before (control) and 60 min after drug administration. Compared to the control phase, hydralazine induced an increase in heart rate and cardiac index (p less than 0.01), and a decrease in mean arterial pressure and pulmonary wedge pressure (p less than 0.01, p less than 0.05, respectively). The hemodynamic effects were associated with increased norepinephrine plasma concentration during upright exercise (p less than 0.05) and increased plasma renin activity (p less than 0.01). After administration of captopril, heart rate at rest (p less than 0.05), mean arterial pressure, and pulmonary wedge pressure decreased significantly (p less than 0.01). Cardiac index remained unchanged. Norepinephrine plasma concentrations were not significantly influenced despite a tendency to lower levels during upright exercise. Plasma renin activity increased (p less than 0.01) and aldosterone at rest decreased significantly (p less than 0.05). These differences in neurohumoral response between both drugs may be important for their long-term effects.

背景与目标： ：为研究肼苯哒嗪和卡托普利在首次给药后的血流动力学和神经体液作用，在一项交叉试验中纳入了15名特发性扩张型心肌病（NYHA II级和III级）患者，洗脱期为3天。通过使用Swan-Ganz热稀释导管测量血流动力学参数，并在给药前（对照）和给药后60分钟，在仰卧休息和标准化直立运动期间对静脉血进行采样。与对照期相比，肼苯哒嗪引起心率和心脏指数增加（p小于0.01），平均动脉压和肺楔压降低（p分别小于0.01和p小于0.05）。血液动力学效应与在直立运动期间增加去甲肾上腺素的血浆浓度（p小于0.05）和增加血浆肾素活性（p小于0.01）有关。服用卡托普利后，静息心率（p小于0.05），平均动脉压和肺楔压显着降低（p小于0.01）。心脏指数保持不变。尽管在直立运动过程中去甲肾上腺素的血浆浓度有降低的趋势，但并未显着影响血浆中的浓度。血浆肾素活性增加（p小于0.01），静止时醛固酮明显降低（p小于0.05）。两种药物之间神经体液反应的这些差异可能对它们的长期作用很重要。

BACKGROUND & AIMS: :Kaposi's sarcoma appeared 8 months after the start of captopril treatment in a 70-year-old woman with rheumatoid arthritis. A marked reduction of cutaneous and gastric lesions occurred when captopril was stopped. These findings are compared to immunosuppressive drug induced forms of Kaposi's sarcoma.

背景与目标： 卡托普利开始治疗8个月后，一名70岁风湿性关节炎妇女出现卡波西肉瘤。卡托普利停药后，皮肤和胃部病变明显减少。将这些发现与免疫抑制药物诱导的卡波西氏肉瘤形式进行比较。

BACKGROUND & AIMS: BACKGROUND:Previous laboratory studies have shown that angiotensin II is produced locally in the rat internal anal sphincter causing potent contraction. The aim of this first human study was to evaluate the safety and manometric effects of topical application of captopril (an ACE inhibitor) on the resting anal pressure in healthy adult volunteers. METHODS:Ten volunteers, mean age 32.5 years (range, 19-48 years), underwent anorectal manometric evaluation of the mean anal resting pressure (MRAP) and the length of the high-pressure zone (HPZ) before 20 and 60 min after topical application of captopril (0.28 %) cream. Cardiovascular variables (systolic blood pressure, diastolic blood pressure and pulse) were measured before and for up to 1 h after cream application. Side effects were recorded. Adverse events and patient comfort after the cream application were evaluated within a 24-h period by completing a questionnaire. RESULTS:There was no significant change overall in MRAP following captopril administration, although in half the patients, there were reductions in MRAP after treatment. Half the patients had a reduction in the mean resting HPZ length; however, there was no overall difference between pre- and post-treatment values. There was no effect on basic cardiovascular parameters and no correlation between manometric and cardiovascular variables. CONCLUSIONS:Topical application of captopril cream may result in a reduction in MRAP in volunteers without anorectal disease. Its use is associated with minimal side effects. It may be a new potential therapeutic option in the treatment of anal fissure. Further studies are required to determine the optimal concentration, dose and frequency of application.

背景与目标： 背景：先前的实验室研究表明，血管紧张素II在大鼠肛门内括约肌中局部产生，引起强力收缩。这项首次人类研究的目的是评估局部应用卡托普利（一种ACE抑制剂）对健康成人志愿者的静息肛门压力的安全性和测压效果。
方法：十名志愿者，平均年龄32.5岁（范围19-48岁），在局部用药后20分钟和60分钟进行肛门直肠测压评估，以评估平均肛门静息压（MRAP）和高压区长度（HPZ）卡托普利（0.28％）霜的应用。在涂抹乳霜之前和之后长达1小时，测量心血管变量（收缩压，舒张压和脉搏）。记录副作用。通过填写问卷调查表，在24小时内评估了使用乳膏后的不良事件和患者的舒适度。
结果：卡托普利给药后MRAP总体上没有显着变化，尽管一半的患者在治疗后MRAP降低。一半的患者的平均静息HPZ长度减少；但是，治疗前和治疗后的值之间没有总体差异。对基本的心血管参数没有影响，测压和心血管变量之间也没有相关性。
结论：卡托普利乳膏的局部应用可导致无肛门直肠疾病的志愿者的MRAP降低。它的使用具有最小的副作用。它可能是治疗肛裂的一种新的潜在治疗选择。需要进一步研究以确定最佳的浓度，剂量和使用频率。

BACKGROUND & AIMS: :The effect of exogenous angiotensin II (A II) and the angiotensin converting enzyme (ACE)-inhibitor captopril on plasma levels of neuropeptide Y-like immunoreactivity (NPY-LI) has been studied in the pithed guinea pig. Four periods of pre-ganglionic nerve stimulation (PNS, 8 Hz for 30s with 20 min intervals) were applied and the increases of mean arterial blood pressure (delta BP), heart rate (delta HR) and plasma NPY-LI (delta NPY-LI) in response to PNS were analysed in non-pre-treated and captopril pre-treated animals. Captopril (5 mg x kg-1 i.v.) reduced basal blood pressure and delta BP by 20% and 11%, respectively. Infusion of A II (0.5 microgram x kg-1 = min-1 i.v.) caused a significant increase in basal and PNS-induced maximal blood pressure response but reduced delta BP in captopril and non-pre-treated animals by 40% and 16%, respectively. A II elicited a long-lasting increase of basal heart rate by 12% but reduced delta HR by 36% in non-pre-treated animals. However, neither captopril alone nor A II infusion to captopril pre-treated animals significantly changed heart-rate values. The effects of exogenous A II on the cardiovascular responses were abolished by the A II-antagonist saralasin (a bolus injection, 40 micrograms x kg-1 i.v. followed by an infusion, 30 micrograms x kg-1 x min-1), which per se had no significant effect. Captopril pre-treatment reduced basal plasma NPY-LI levels by 38% and delta NPY-LI by 46% in response to PNS 1. However, neither in non-pre-treated nor in captopril pre-treated animals did infusion of A II significantly change the plasma NPY-LI level.(ABSTRACT TRUNCATED AT 250 WORDS)

背景与目标： ：在有髓的豚鼠中研究了外源性血管紧张素II（A II）和血管紧张素转化酶（ACE）抑制剂卡托普利对血浆神经肽Y样免疫反应性（NPY-LI）的影响。施加了四个时期的神经节前神经刺激（PNS，8 Hz，持续30s，间隔20分钟），并且平均动脉血压（delta BP），心率（delta HR）和血浆NPY-LI（delta NPY-在非预处理和卡托普利预处理的动物中分析了响应PNS的L1）。卡托普利（5 mg x kg-1 i.v.）分别使基础血压和BP降低20％和11％。输注A II（0.5微克x kg-1 = min-1 iv）导致基础和PNS诱导的最大血压反应显着增加，但卡托普利和未经预处理的动物的δBP降低了40％和16％ ， 分别。在未进行预处理的动物中，II引起基础心率持久提高12％，但降低HR降低36％。但是，单独使用卡托普利或向卡托普利预处理的动物中输注A II均不会显着改变心率值。 A II拮抗剂撒拉辛消除了外源性A II对心血管反应的影响（推注40毫克x kg-1静脉推注，然后输注30毫克x kg-1 x min-1）， se没有明显作用。卡托普利预处理可响应PNS 1降低38％的基础血浆NPY-LI水平和46％的δNPY-LI水平。但是，在未进行预处理的动物和在卡托普利预处理的动物中，A II的注入量均未显着更改血浆NPY-LI水平。（摘要以250字截断）

BACKGROUND & AIMS: :In this work, near-infrared spectroscopy (NIRS) method was used to evaluate the uniformity of dosage units of three captopril 25 mg tablets commercial batches. The performance of the calibration method was assessed by determination of Q value (0.9986), standard error of estimation (C-set SEE = 1.956), standard error of prediction (V-set SEP = 2.076) as well as the consistency (106.1%). These results indicated the adequacy of the selected model. The method validation revealed the agreement of the reference high pressure liquid chromatography (HPLC) and NIRS methods. The process evaluation using the NIRS method showed that the variability was due to common causes and delivered predictable results consistently. Cp and Cpk values were, respectively, 2.05 and 1.80. These results revealed a non-centered process in relation to the average target (100% w/w), in the specified range (85-115%). The probability of failure was 21:100 million tablets of captopril. The NIRS in combination with the method of multivariate calibration, partial least squares (PLS) regression, allowed the development of methodology for the uniformity of dosage units evaluation of captopril tablets 25 mg. The statistical process control strategy associated with NIRS method as PAT played a critical role in understanding of the sources and degree of variation and its impact on the process. This approach led towards a better process understanding and provided the sound scientific basis for its continuous improvement.

背景与目标： ：在这项工作中，使用近红外光谱（NIRS）方法评估了三批卡托普利25mg片剂商业批次的剂量单位的均一性。通过确定Q值（0.9986），估计的标准误差（C-set SEE = 1.956），预测的标准误差（V-set SEP = 2.076）以及一致性（106.1％）来评估校准方法的性能）。这些结果表明所选模型的适当性。方法验证表明参考高压液相色谱（HPLC）和NIRS方法具有一致性。使用NIRS方法进行的过程评估表明，变异性是由于常见原因引起的，并且始终如一地提供了可预测的结果。 Cp和Cpk值分别为2.05和1.80。这些结果表明，相对于平均目标（100％w / w），在指定范围（85％至115％）中，存在一个非中心过程。失败的可能性是卡托普利21：1亿片。 NIRS与多变量校准，偏最小二乘（PLS）回归方法相结合，为开发25μmg卡托普利片的剂量单位评估的均一性提供了方法。与NIRS方法（如PAT）相关的统计过程控制策略在理解变异的来源和程度及其对过程的影响方面起着至关重要的作用。这种方法使人们对过程有了更好的理解，并为其不断改进提供了可靠的科学依据。

BACKGROUND & AIMS: :Angiotensin converting enzyme inhibitors reduce blood pressure without reflex tachycardia, possibly as a result of enhanced hypothesis that this results from the removal of the parasympathetic activity. We examined the vagolytic action of angiotensin II or alternatively by acetylcholinesterase inhibition. Both captopril and [Sar1ala8] angiotensin II, (saralasin), caused modest falls in blood pressure, without increasing heart rate in normotensive subjects. Captopril and saralasin significantly attenuated the vagally mediated heart rate slowing after facial immersion in water. There was a close correlation between the effects produced by captopril and saralasin on the diving reflex. Infusion of subpressor doses of angiotensin II, reversed the hypotensive effect of captopril and returned the bradycardia after facial immersion to placebo level. In vitro neither captopril nor enalapril or lisinopril affected bovine erythrocyte acetylcholinesterase activity. The parasympathetic effect of angiotensin converting enzyme inhibitors appear to reflect a direct consequence of the removal of angiotensin II.

背景与目标： ：血管紧张素转换酶抑制剂可降低血压而无反射性心动过速，这可能是由于假说交感神经活动被消除导致假说增强的结果。我们检查了血管紧张素II或通过乙酰胆碱酯酶抑制的迷走神经作用。卡托普利和[Sar1ala8]血管紧张素II（萨拉生素）均引起血压适度下降，而血压正常者的心率却没有增加。卡托普利和撒拉辛在面部浸入水中后可显着减弱阴道介导的心率减慢。卡托普利和萨拉信素对潜水反射产生的影响之间存在密切的相关性。输注低于剂量的血管紧张素II，可逆转卡托普利的降压作用，并使面部浸入后的心动过缓恢复至安慰剂水平。在体外，卡托普利，依那普利或赖诺普利均不影响牛红细胞乙酰胆碱酯酶活性。血管紧张素转化酶抑制剂的副交感作用似乎反映了血管紧张素II去除的直接后果。

BACKGROUND & AIMS: BACKGROUND:The presence of diastolic dysfunction in a hypertensive patient is not necessarily associated to the existence of left ventricular hypertrophy. The aim of this study was to determine whether the reduction of the left ventricular mass in hypertensive patients treated with captopril is accompanied by an improvement of the diastolic filling indexes. METHODS:Nineteen patients with essential hypertension were studied before and after one year of treatment with captopril. Different morphological indexes and diastolic function of the left ventricle were evaluated by mode M and Doppler echography. RESULTS:The indexes of left ventricular mass diminished significantly with treatment with captopril. The thickness of the ventricular walls diminished with treatment although not significantly. No significant modification was observed in the indexes of diastolic function (quotient of speed of protodiastolic filling/speed of telediastolic filling and time of deceleration of transmitral fluid during diastole) following the treatment period. CONCLUSIONS:Diminution of the left ventricular mass induced by captopril in hypertensive patients is not accompanied by an improvement in ventricular filling. It is suggested that myocardial hypertrophy is not responsible for diastolic dysfunction of arterial hypertension.

背景与目标： 背景：高血压患者舒张功能障碍的存在不一定与左心室肥大的存在有关。这项研究的目的是确定在接受卡托普利治疗的高血压患者中左心室重量的减少是否伴随着舒张期充盈指数的改善。
方法：对19例原发性高血压患者在卡托普利治疗前后进行了研究。 M型和多普勒超声检查评估左心室的不同形态学指标和舒张功能。
结果：卡托普利治疗可使左心室质量指标明显降低。心室壁的厚度随着治疗而减小，尽管没有显着减小。在治疗期之后，在舒张功能指标（舒张期充盈速度/舒张期充盈速度和舒张期传输液减速时间的商）中未观察到明显的改变。
结论：卡托普利可减轻高血压患者的左心室质量，但并不能改善心室充盈。提示心肌肥大与动脉高血压的舒张功能障碍无关。

BACKGROUND & AIMS: :Both captopril renal scintigraphy (CRS) and conventional arteriography were retrospectively evaluated in 64 patients to study CRS efficacy in hypertensive patients with multiple renal arteries (MRA). The presence of MRA was angiographically demonstrated in 9 patients, 7 unilaterally and 2 bilaterally, with a total of 11 kidneys supplied by 2 or more arteries. Overall, 25 MRA were identified and 7 were affected by stenosis of > 50%, causing a reduction of arterial supply in 5 of 11 kidneys. CRS correctly diagnosed all five ischemic kidneys (true positives) and five of six nonischemic kidneys (true negatives); in one case in which perfusion was not reduced, the CRS diagnosis was falsely positive. In the presence of MRA, CRS proved effective in identifying renal artery stenosis of > 50%, involving either one or all the MRA. This study shows that the presence of MRA is not a drawback in the evaluation of renal artery stenosis by means of CRS.

背景与目标： ：回顾性分析了64例患者的卡托普利肾闪烁显像（CRS）和常规动脉造影，以研究CRS在高血压多肾动脉（MRA）患者中的疗效。 9例患者通过血管造影证实了MRA的存在，其中单侧7例，双侧2例，共有11条肾脏由2条或更多条动脉供血。总体上，鉴定出25个MRA，其中7个受狭窄> 50％的影响，导致11个肾脏中的5个肾脏的动脉供应减少。 CRS正确诊断了全部五个缺血性肾脏（真阳性）和六个非缺血性肾脏中的五个（真阴性）；在没有减少灌注的情况下，CRS诊断为假阳性。在存在MRA的情况下，CRS被证明可有效地识别≥50％的肾动脉狭窄，涉及一个或全部MRA。这项研究表明，在通过CRS评估肾动脉狭窄方面，MRA的存在并不是缺点。

BACKGROUND & AIMS: BACKGROUND:Acute administration of cocaine leads to left ventricular dysfunction and a decrease in coronary blood flow. This experiment studied the relationship between function and flow over time in cocaine heart disease and examined the effects of captopril on this relationship. METHODS:Dogs anesthetized with pentobarbital (n = 13) were given a 3 mg/kg body weight intravenous bolus of cocaine followed by a 7 mg/kg infusion over 10 minutes. Animals were then randomly assigned to receive either captopril (0.5 mg/kg infused over 5 minutes, followed by 0.5 mg/kg/h) or an equivalent volume of saline beginning 15 minutes after cocaine administration. Coronary blood flow (radioactive microspheres and Doppler flow probes) and left ventricular function (two-dimensional echocardiogram and dP/dt) were monitored for 2 hours. RESULTS:Within 15 minutes, cocaine caused a drop in dP/dt by 39% to 42% and in coronary blood flow by 35%. Cocaine also caused an increase in left ventricular end-diastolic pressures in both groups. Cocaine resulted in prolongation of an index of end-diastolic isovolumic relaxation time (tau) from a baseline of 34 milliseconds to 56 milliseconds at 15 minutes after cocaine administration in the control group and from a baseline of 35 milliseconds to 49 milliseconds in the captopril group (P < 0.05). By 2 hours after therapy, the tau in the control group remained elevated, whereas in the captopril group it returned toward baseline. At 2 hours of observation, systolic function recovered while coronary flow remained depressed. There was no difference between the captopril and control groups in coronary blood flow or systolic cardiac function at any time during the study. CONCLUSIONS:Cocaine caused left ventricular systolic and diastolic dysfunction as well as reduced coronary blood flow. At 2 hours there is a dissociation of systolic function, which recovers, and of coronary blood flow, which does not. Captopril had no effect on coronary blood flow or systolic left ventricular function following cocaine administration.

背景与目标： 背景：可卡因的急性给药导致左心功能不全和冠状动脉血流减少。该实验研究了可卡因心脏病患者的功能和血流随时间的关系，并研究了卡托普利对这种关系的影响。
方法：对戊巴比妥麻醉的狗（n = 13）给予3 mg / kg体重的可卡因静脉推注，然后在10分钟内输注7 mg / kg。然后将动物随机分配为在服用可卡因后15分钟开始接受卡托普利（0.5 mg / kg输注5分钟，然后输注0.5 mg / kg / h）或等体积的盐水。监测冠状动脉血流量（放射性微球和多普勒血流探头）和左心室功能（二维超声心动图和dP / dt）持续2小时。
结果：在15分钟内，可卡因使dP / dt下降了39％至42％，冠状动脉血流量下降了35％。可卡因还引起两组左心室舒张末期压力的升高。可卡因导致对照组的可卡因给药后舒张末期等容舒张时间指数从34毫秒延长至56毫秒，卡托普利组从35毫秒延长至49毫秒（P ＜0.05）。到治疗后2小时，对照组的tau仍然升高，而卡托普利组的tau恢复到基线。观察2小时后，收缩功能恢复，而冠状动脉血流却保持下降。在研究过程中的任何时候，卡托普利和对照组之间的冠状动脉血流量或心脏收缩功能均无差异。
结论：可卡因引起左心室收缩和舒张功能障碍以及冠状动脉血流量减少。在2小时时，收缩功能恢复正常，而冠状动脉血流没有恢复。可卡因给药后，卡托普利对冠状动脉血流或收缩期左心室功能无影响。

BACKGROUND & AIMS: :To explore the effects of angiotensin-converting enzyme (ACE) inhibitors on endothelial dysfunction induced by homocysteine thiolactone (HTL). Both endothelium-dependent relaxation and nondependent relaxation of thoracic aortic rings in rats induced by acetylcholine (Ach) or sodium nitroprusside (SNP) and biochemical parameters including malondialdehyde (MDA) and nitric oxide (NO) were measured in rat isolated aorta. Exposure of aortic rings to HTL (3 to 30 mM) for 90 minutes made a significant inhibition of endothelium-dependent relaxation induced by Ach, decreased contents of NO, and increased MDA concentration in aortic tissue. After incubation of aortic rings with captopril (0.003 to 0.03 mM) attenuated the inhibition of endothelium-dependent relaxation (EDR) and significantly resisted the decrease of NO content and elevation of MDA concentration caused by HTL (30 mmol/L) in aortic tissues, a similarly protective effect was observed when the aortic rings were incubated with both N-acetylcysteine (0.05 mM). Treatment with enalaprilat (0.003 to 0.01 mM) made no significant difference with the HTL (30 mM) group regarding EDR, but enalaprilat (0.03 mM) and losartan (0.03 mM) could partly restore the EDR in response to HTL (30 mM). Captopril was more effective than enalaprilat and losartan in attenuation of the inhibition of on acetylcholine-stimulated aortic relaxation by HTL in the same concentration. Moreover, superoxide dismutase (SOD, 200 U/mL), which is a scavenger of superoxide anions, apocynin (0.03 mM), which is an inhibitor of NADPH oxidase, and l-Arginine (3 mmol/L), a precursor of nitric oxide (NO), could reduce HTL (30 mM)-induced inhibition of EDR. After pretreatment with not only the NO synthase inhibitor Nomega-nitro-l-arginine methyl ester (L-NAME, 0.01 mM) but also the free sulfhydryl group blocking agent p-hydroxymercurybenzoate (PHMB, 0.05 mM) could abolish the protection of captopril and N-acetylcysteine, respectively. These results suggest that mechanisms of endothelial dysfunction induced by HTL may include the decrease of NO and the generation of oxygen free radicals and that captopril can restore the inhibition of EDR induced by HTL in isolated rat aorta, which may be related to scavenging oxygen free radicals and may be sulfhydryl-dependent.

背景与目标： ：探讨血管紧张素转换酶（ACE）抑制剂对高半胱氨酸硫代内酯（HTL）诱导的内皮功能障碍的影响。在大鼠离体主动脉中，测量了乙酰胆碱（Ach）或硝普钠（SNP）诱导的大鼠胸主动脉环的内皮依赖性舒张和非依赖性舒张以及包括丙二醛（MDA）和一氧化氮（NO）在内的生化参数。将主动脉环暴露于HTL（3至30 mM）90分钟可显着抑制Ach诱导的内皮依赖性舒张，减少NO含量并增加主动脉组织中的MDA浓度。用卡托普利（0.003至0.03 mM）孵育主动脉环后，减弱了对血管内皮依赖性舒张（EDR）的抑制作用，并显着抑制了HTL（30 mmol / L）引起的NO含量降低和MDA浓度升高，当主动脉环与两个N-乙酰半胱氨酸（0.05 mM）一起孵育时，观察到类似的保护作用。依那普利拉（0.003至0.01 mM）的治疗与HTL（30 mM）组在EDR方面无显着差异，但依那普利拉（0.03 mM）和氯沙坦（0.03 mM）可以部分响应HTL（30 mM）恢复EDR。在相同浓度下，卡托普利比依那普利拉和氯沙坦更有效地抑制HTL对乙酰胆碱刺激的主动脉舒张的抑制作用。此外，作为超氧化物阴离子的清除剂的超氧化物歧化酶（SOD，200 U / mL），作为NADPH氧化酶抑制剂的载脂蛋白（0.03 mM）和作为硝酸前体的l-精氨酸（3 mmol / L）。一氧化氮（NO）可以降低HTL（30 mM）对EDR的抑制作用。用NO合酶抑制剂Nomega-硝基-1-精氨酸甲酯（L-NAME，0.01 mM）预处理后，游离巯基封闭剂对羟基汞基苯甲酸酯（PHMB，0.05 mM）都可以取消卡托普利和N-乙酰半胱氨酸分别。这些结果表明，HTL诱导的内皮功能障碍的机制可能包括NO的减少和氧自由基的产生，并且卡托普利可以恢复HTL诱导的离体大鼠主动脉对EDR的抑制作用，这可能与清除氧自由基有关。并且可能是巯基依赖性的。