• 【激肽对卡托普利在兔肾血管舒张作用中的作用。】 复制标题 收藏 收藏
    DOI:10.1161/01.hyp.17.4.504 复制DOI
    作者列表:Hajj-ali AF,Zimmerman BG
    BACKGROUND & AIMS: :This study was conducted to examine the role of bradykinin in the persistence of the renal vasodilator effect of captopril during angiotensin II receptor blockade. Blood pressure and renal blood flow were monitored in eight groups of pentobarbital-anesthetized rabbits. In group 4, captopril alone was administered, and it decreased blood pressure by 14 +/- 4 mm Hg and increased renal blood flow by 21 +/- 4 ml/min. After a bolus injection and a constant intravenous infusion of the imidazole derivative angiotensin II receptor antagonist DuP 753 (group 5), captopril decreased blood pressure by 9 +/- 2 mm Hg and increased renal blood flow by 8 +/- 1 ml/min (12 +/- 1% change in renal blood flow, p less than 0.05 versus group 4). In the presence of a constant intravenous infusion of saralasin (group 6), captopril decreased blood pressure by 13 +/- 5 mm Hg and increased renal blood flow by 7 +/- 2 ml/min (17 +/- 5% change in renal blood flow, p less than 0.05 versus group 4). These results did not differ from those in group 5. During a constant intrarenal arterial infusion of a B2 bradykinin receptor antagonist, DArg0, [Hyp3-Thi5,8-DPhe7]-bradykinin (BkA) (group 7), captopril decreased blood pressure by 14 +/- 4 mm Hg and increased renal blood flow by 10 +/- 4 ml/min. Combined administration of DuP 753 intravenously and BkA intra-arterially (group 8) eliminated the effect of captopril. In group 8, captopril caused insignificant changes in blood pressure and renal blood flow. The results indicate that DuP 753 and saralasin antagonize the renin-angiotensin system to a comparable extent in vivo. Although blockade of the latter system accounted for a significant part of the increase in renal blood flow caused by captopril, the remaining component was contributed by endogenous bradykinin.
    背景与目标: :本研究旨在检查缓激肽在血管紧张素II受体阻断期间卡托普利对肾脏血管舒张作用的持续作用中的作用。在八组戊巴比妥麻醉的兔子中监测血压和肾血流量。在第4组中,单独使用卡托普利,它使血压降低了14 4 mm Hg,并使肾血流量增加了21 4 ml / min。推注并持续静脉注射咪唑衍生物血管紧张素II受体拮抗剂DuP 753(第5组)后,卡托普利可使血压降低9 /-2 mm Hg,并使肾血流量增加8 /-1 ml / min(12 /-肾血流量变化1%,与第4组相比,p小于0.05。在持续不断地静脉注射撒拉辛(第6组)的情况下,卡托普利可使血压降低13 /-5 mm Hg,并使肾血流量增加7 /-2 ml / min(肾血流量变化17 /-5%) ,与第4组相比,p小于0.05)。这些结果与第5组没有差异。在恒定的肾动脉内输注B2缓激肽受体拮抗剂DArg0,[Hyp3-Thi5,8-DPhe7]-缓激肽(BkA)(第7组)期间,卡托普利可通过14 /-4 mm Hg和增加10 /-4 ml / min的肾血流量。静脉内联合DuP 753和动脉内BkA联合给药(第8组)消除了卡托普利的作用。在第8组中,卡托普利引起的血压和肾脏血流变化不明显。结果表明,DuP 753和aralasin在体内具有相当程度的拮抗肾素-血管紧张素系统的作用。尽管后一种系统的阻断在卡托普利引起的肾血流量增加中占了很大一部分,但其余成分是由内源性缓激肽引起的。
  • 【卡托普利和依卡替班对角叉菜胶诱发的水肿中缓激肽(BK)和des [Arg9] BK的影响。】 复制标题 收藏 收藏
    DOI:10.1016/0196-9781(96)00145-3 复制DOI
    作者列表:Decarie A,Adam A,Couture R
    BACKGROUND & AIMS: The effects of captopril, an angiotensin-converting enzyme inhibitor (ACEI), and a selective B2 kinin receptor antagonist (Icatibant) were examined on the paw edema and tissue contents of bradykinin (BK) and des[Arg9]BK following the intraplantar injection of carrageenan in rats. To this end, BK-like immunoreactivity (BK-LI) and des[Arg9]BK-LI were measured with highly sensitive and specific chemiluminescent enzyme immunoassays. Because pentobarbital significantly reduced the carrageenan-induced edema between 3 and 8 h, experiments were conducted in conscious rats. Icatibant (32.5 nmol/paw; intraplantar) significantly reduced carrageenan-induced paw edema between 3 and 8 h in captopril-untreated rats and at 1 and 3 h in captopril-treated rats (0.2 mg/kg x 5 days, per os). The paw content of BK-LI was increased 10-fold in captopril-untreated and 29-fold in captopril-treated rats 1 h after carrageenan injection. In parallel, des[Arg9]BK-LI was increased 8-fold in captopril-untreated and 24-fold in captopril-treated rats. Icatibant prevented the maximal increases in BK-LI and des[Arg9]BK-LI induced by carrageenan. It is concluded that inhibition of ACE by captopril enhanced the early production of endogenous BK and the edema formation induced by carrageenan through a B2 receptor-mediated mechanism. However, the B2 receptor does not appear to be involved in the late phase of the inflammatory response (from 5 to 24 h) to carrageenan in rats pretreated with ACEI. Although the concentrations of des[Arg9]BK were greater than those of BK, it is unlikely that B1 receptors play a significant role in this model of carrageenan-induced edema.

    背景与目标: 足底注射异丙酚后,检查了卡托普利,血管紧张素转换酶抑制剂(ACEI)和选择性B2激肽受体拮抗剂(Icatibant)对爪水肿和缓激肽(BK)和des [Arg9] BK的组织含量的影响。大鼠中的角叉菜胶。为此,用高灵敏度和特异性的化学发光酶免疫测定法测量了BK样免疫反应性(BK-LI)和des [Arg9] BK-LI。由于戊巴比妥可在3至8小时内显着减少角叉菜胶引起的水肿,因此在有意识的大鼠中进行了实验。伊卡替班(32.5 nmol /爪;足底内)在未经卡托普利治疗的大鼠中3至8小时以及经卡托普利治疗的大鼠1至3小时内均显着减少了角叉菜胶诱导的爪水肿(0.2 mg / kg x 5天,每次口服)。角叉菜胶注射后1小时,未经卡托普利治疗的大鼠的BK-LI的爪子含量增加10倍,而经卡托普利治疗的大鼠的BK-LI的爪子含量增加29倍。平行地,在未经卡托普利治疗的大鼠中,des [Arg9] BK-LI增加了8倍,而在经卡托普利治疗的大鼠中,des [Arg9] BK-LI增加了24倍。伊卡替班预防了由角叉菜胶诱导的BK-LI和des [Arg9] BK-LI的最大增加。结论是,卡托普利对ACE的抑制作用通过B2受体介导的机制增强了内源性BK的早期产生和角叉菜胶诱导的水肿形成。但是,在用ACEI预处理的大鼠中,B2受体似乎不参与对角叉菜胶的炎症反应的后期(5至24小时)。尽管des [Arg9] BK的浓度高于BK的浓度,但B1受体不太可能在这种由角叉菜胶诱发的水肿模型中发挥重要作用。

  • 【卡托普利肾造影和经皮腔内血管成形术对94例肾动脉狭窄患者的血压影响。】 复制标题 收藏 收藏
    DOI:10.1093/ajh/4.12.685s 复制DOI
    作者列表:Geyskes GG,de Bruyn AJ
    BACKGROUND & AIMS: :We treated 94 patients by percutaneous transluminal angioplasty (PTA) for renal artery stenosis (RAS). Prior to PTA, a renogram during angiotensin converting enzyme (ACE) inhibition with captopril was performed, but the result did not influence the decision to treat. The parenchymal time activity curves were judged by visual interpretation. Of the 94 patients, 51 had unilateral and 43 bilateral RAS. In 17 patients with bilateral RAS, PTA could be performed only in the least affected kidney; because of this the effect of PTA on their blood pressure could not be evaluated. Of the remaining 77 patients, a positive captopril renogram was seen in all 31 cured patients, in 22 of the 27 patients with improvement, and in six of the 19 patients with no change of their blood pressure. The sensitivity of the tests for cure and improvement of the blood pressure was 91% (53/58 patients) for all patients, 95% in patients with unilateral RAS (35/37), and 86% (18/21 patients) in patients with bilateral RAS, bilaterally treated. In 18 patients with a negative captopril renogram the blood pressure improved in five, and did not change in 13 patients. The success of PTA in patients with a negative captopril renogram was so poor that we feel it would have been better not to have performed angiography and PTA at all. In conclusion, captopril renography is a useful investigation in assessing the likelihood of blood pressure reduction after PTA of renal artery stenosis.
    背景与目标: :我们通过经皮腔内血管成形术(PTA)治疗了94例肾动脉狭窄(RAS)患者。在进行PTA之前,在用卡托普利抑制血管紧张素转化酶(ACE)的过程中进行了肾图检查,但结果并未影响治疗决定。实质时间活动曲线通过视觉解释来判断。在94例患者中,有51例为单侧RAS,有43例为双侧RAS。在17例双侧RAS患者中,仅可在受影响最小的肾脏中进行PTA。因此,无法评估PTA对他们的血压的影响。在其余的77例患者中,所有31例治愈的患者,27例好转的患者中有22例,血压没有变化的19例中的6例均显示卡托普利肾图检查阳性。所有患者对治愈和改善血压的测试的敏感性分别为91%(53/58患者),单侧RAS患者(95/35)和95%(18/21患者)双侧RAS,双侧治疗。卡托普利肾电图阴性的18例患者中,有5例血压有所改善,而13例患者中血压没有变化。卡托普利肾电图阴性的患者中PTA的成功非常差,以至于完全不进行血管造影和PTA会更好。总之,卡托普利肾造影是一项有用的研究,可用于评估PTA肾动脉狭窄后血压降低的可能性。
  • 【氯沙坦与卡托普利的比较对有症状心力衰竭患者死亡率的影响:一项随机试验-氯沙坦心力衰竭生存研究ELITE II。】 复制标题 收藏 收藏
    DOI:10.1016/s0140-6736(00)02213-3 复制DOI
    作者列表:Pitt B,Poole-Wilson PA,Segal R,Martinez FA,Dickstein K,Camm AJ,Konstam MA,Riegger G,Klinger GH,Neaton J,Sharma D,Thiyagarajan B
    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)。
  • 【卡托普利和依那普利清除自由基的活性比较:高血压糖尿病患者体内研究三个月。】 复制标题 收藏 收藏
    DOI: 复制DOI
    作者列表:Bain SC,Le Guen CA,Lunec J,Barnett AH
    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。
  • 【卡托普利(一种血管紧张素转化酶抑制剂)对大鼠吗啡镇痛和耐受性的影响,并通过这种作用阐明了炎症和内质网应激途径。】 复制标题 收藏 收藏
    DOI:10.1016/j.neulet.2020.135504 复制DOI
    作者列表:Taskiran AS,Avci O
    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。
  • 【卡托普利不会在人充血性心力衰竭中急性调节血浆血浆内皮素-1的浓度。】 复制标题 收藏 收藏
    DOI:10.1007/BF00050997 复制DOI
    作者列表:Grenier O,Pousset F,Isnard R,Kalotka H,Carayon A,Maistre G,Lechat P,Guerot C,Thomas D,Komajda M
    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。

  • 【卡托普利对氟烷麻醉的硝普钠钠引起的低血压期间肾素-血管紧张素系统和交感神经系统的影响。】 复制标题 收藏 收藏
    DOI:10.1097/00005344-199003000-00017 复制DOI
    作者列表:Stead SW,Bloor BC
    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)
  • 【对肼屈嗪和卡托普利的血流动力学和神经体液反应:特发性扩张型心肌病的对照研究。】 复制标题 收藏 收藏
    DOI:10.1097/00005344-198700002-00011 复制DOI
    作者列表:Schofer J,Mathey DG,Polster J,Bode V,Dietlein G
    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。
  • 【类风湿关节炎患者的卡波西肉瘤可能是卡托普利在病变发展中的责任。】 复制标题 收藏 收藏
    DOI: 复制DOI
    作者列表:Larbre JP,Nicolas JF,Collet P,Larbre B,Llorca G
    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。
  • 【局部肛门卡托普利对健康志愿者静息肛门压力的影响:第一个人类先导研究。】 复制标题 收藏 收藏
    DOI:10.1007/s10151-013-0986-y 复制DOI
    作者列表:Khaikin M,Bashankaev B,Sands D,Weiss EG,Zbar A,Wexner SD
    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。
  • 【卡托普利对有髓豚鼠的血浆神经肽Y(NPY)免疫反应水平的影响。】 复制标题 收藏 收藏
    DOI:10.1016/0143-4179(91)90144-8 复制DOI
    作者列表:Dahlöf P,Lundberg JM,Dahlöf C
    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)
  • 【近红外光谱和统计过程控制(SPC)策略对卡托普利片(25mg)制造过程理解的关键作用:一个案例研究。】 复制标题 收藏 收藏
    DOI:10.3109/10837450.2013.867448 复制DOI
    作者列表:Curtivo CP,Funghi NB,Tavares GD,Barbosa SF,Löbenberg R,Bou-Chacra NA
    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。
  • 【卡托普利对反射控制心率的影响:可能的机制。】 复制标题 收藏 收藏
    DOI:10.1111/j.1365-2125.1985.tb02793.x 复制DOI
    作者列表:Ajayi AA,Campbell BC,Meredith PA,Kelman AW,Reid JL
    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。
  • 【卡托普利对原发性高血压患者左心室形态和功能的影响】 复制标题 收藏 收藏
    DOI: 复制DOI
    作者列表:Laviades C,Mayor G,Díez J
    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。

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