Hemodynamic effects of renin inhibition by enalkiren in chronic congestive heart failure.
Hemodynamic effects of renin inhibition by enalkiren in chronic congestive heart failure.
复制标题
依那吉伦抑制肾素对慢性充血性心力衰竭的血流动力学影响。
DOI：
10.1016/0002-9149(91)90101-p
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Packer,M
中科院分区：
文献类型：
--
作者：
Neuberg,GW;Kukin,ML;Penn,J;Medina,N;Yushak,M;Packer,M
先前对慢性充血性心力衰竭（CHF）患者肾素-血管紧张素系统的阻断主要集中在该系统的2个远端部位，即血管紧张素转换酶和血管紧张素II受体。然而，最近的工作已经导致了直接抑制肾素的药物的发展，肾素是级联反应的最近一步。在这项研究中，我们研究了enalkiren对9例慢性CHF患者肾素抑制的血流动力学影响。enalkiren是一种灵长类动物选择性的二肽肾素抑制剂，先前已被证明可以抑制血浆肾素活性并降低高血压患者的血压。急性静脉enalkiren管理局(1.0毫克/公斤)生产增加心脏指数(2.0±0.3,2.3±0.1升/分钟/ m2)和中风容积指数(26±3 - 34±4毫升/ m2)和左心室充盈压力的减少(31±3 - 25±3毫米汞柱),意思是右心房压力(15±1到13±2毫米汞柱),心率(78±5到72±6胜/分钟)和系统性血管阻力(2199±594到1339±230达因·s·厘米−5)(p < 0.01 ~ 0.05)。这些观察结果表明，肾素抑制对慢性CHF患者的血流动力学有益，并可能为干扰该疾病患者的肾素-血管紧张素系统提供一种新的方法。
Previous efforts to block the renin-angiotensin system in patients with chronic congestive heart failure (CHF) have focused on 2 distal sites in the system, the angiotensin-converting enzyme and the angiotensin II receptor. Recent work, however, has led to the development of agents that directly inhibit renin, the proximal step in the cascade. In this study, we investigated the hemodynamic effects of renin Inhibition In 9 patients with chronic CHF by using enalkiren, a primate-selective, dipeptide renin inhibitor, which has been previously shown to suppress plasma renin activity and to lower blood pressure in hypertensive patients. The acute intravenous administration of enalkiren (1.0 mg/kg) produced increases in cardiac index (2.0 ± 0.3 to 2.3 ± 0.1 liter/min/m2) and stroke volume index (26 ± 3 to 34 ± 4 ml/m2) and decreases in left ventricular filling pressure (31 ± 3 to 25 ± 3 mm Hg), mean right atrial pressure (15 ± 1 to 13 ± 2 mm Hg), heart rate (78 ± 5 to 72 ± 6 beats/min) and systemic vascular resistance (2,199 ± 594 to 1,339 ± 230 dynes·s·cm−5) (all p < 0.01 to 0.05). These observations indicate that renin inhibition produces hemodynamic benefits in patients with chronic CHF and could potentially provide a novel approach to interfering with the renin-angiotensin system in patients with this disorder.