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卡托普利治疗高血压患者的临床研究。

Clinical studies with captopril treatment of hypertensive patients.

作者信息

Varga K, Alföldi S, Kiss I, Simkó K, Farsang C

机构信息

Second Department of Medicine, Semmelweis University Medical School, Budapest, Hungary.

出版信息

Acta Physiol Hung. 1988;72 Suppl:67-78.

PMID:2855293
Abstract

Haemodynamic and humoral effects of captopril were studied in patients with essential and renovascular hypertension. Captopril decreased significantly both systolic and diastolic blood pressure and moderately, it reduced also the heart rate. On the basis of the haemodynamic effects our patients could be divided into two groups: in patients where the total peripheral resistance (TPR) exceeded 2000 dyn x sec x cm-5 during rest, captopril exerted its hypotensive effect by decreasing TPR. In patients in whom TPR was lower, the hypotensive action could be attributed to the reduction of cardiac output (CO). Captopril increased plasma renin activity, and decreased the activity of angiotensin converting enzyme (ACE) in the plasma. In acute study captopril did not influence plasma noradrenaline level but increased it during long-term administration. It did not affect dopamine or adrenaline levels. Captopril had no effect on plasma beta-endorphin concentration, moreover, the opiate antagonist, naloxone, failed to antagonize its antihypertensive effect. Comparing the acute effects of Capoten (Squibb, USA) and Tensiomin (EGIS, HUNGARY) no significant differences were found.

摘要

在原发性高血压和肾血管性高血压患者中研究了卡托普利的血流动力学和体液效应。卡托普利显著降低收缩压和舒张压,且适度降低心率。基于血流动力学效应,我们的患者可分为两组:在静息时总外周阻力(TPR)超过2000达因×秒×厘米⁻⁵的患者中,卡托普利通过降低TPR发挥其降压作用。在TPR较低的患者中,降压作用可归因于心输出量(CO)的降低。卡托普利增加血浆肾素活性,并降低血浆中血管紧张素转换酶(ACE)的活性。在急性研究中,卡托普利不影响血浆去甲肾上腺素水平,但在长期给药期间会使其升高。它不影响多巴胺或肾上腺素水平。卡托普利对血浆β-内啡肽浓度无影响,此外,阿片拮抗剂纳洛酮未能拮抗其降压作用。比较卡托普利(美国施贵宝公司)和天诺敏(匈牙利EGIS公司)的急性效应,未发现显著差异。

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