Role of the Renin-Angiotensin System in the Systemic Vasoconstriction of Chronic Congestive Heart Failure
Role of the Renin-Angiotensin System in the Systemic Vasoconstriction of Chronic Congestive Heart Failure
复制标题
肾素-血管紧张素系统在慢性充血性心力衰竭全身血管收缩中的作用
作者：
Carl Curtiss;J. Cohn;T. Vrobel;J. Franciosa
摘要 在 15 名患有严重慢性左心室衰竭的患者中，血浆肾素活性 (PRA) 范围广泛，为 0.2-39 ng/ml/hr。 PRA水平与心输出量（CO）或肺动脉楔压（PWP）无关，但与平均动脉压（MAP）（r = -0.45）和全身血管阻力（SVR）（r = -0.40）呈轻微负相关。输注血管紧张素转换酶抑制剂替普肽 (SQ 20,881) 后，PWP 从 26.3 ± 1.3 (SEM) 下降至 20.3 ± 1.4 mm Hg (P < 0.001)，CO 从 3.94 ± 0.23 上升至 4.75 ± 0.31 1/min (P < 0.001)，MAP 从87.5±3.8至77.9±4.1 mm Hg (P < 0.001) 和 SVR 从 1619 ± 148 到 1252 ± 137 dyne-sec-cm-5 (P < 0.001)。 MAP 和 SVR 的下降与对照 PRA 显着相关（分别为 r = 0.68 和 r = 0.58）。当根据对照 PRA 对受试者进行分组时，高肾素组对替普肽的血流动力学反应最大。替普肽治疗后 PRA 上升（8.7 ± 3.4 至 37.9 + 7.7 ng/ml/hr，P < 0.05），但血浆去甲肾上腺素下降（619.1 ± 103.6 至 449.7 ± 75.7，P < 0.05）。因此，肾素-血管紧张素系统似乎在某些心力衰竭患者的 SVR 升高中发挥着重要作用。应探索长期抑制转化酶作为一种可能的治疗方法。
SUMMARY In 15 patients with severe chronic left ventricular failure, plasma renin activity (PRA) ranged widely, from 0.2-39 ng/ml/hr. The level of PRA was unrelated to cardiac output (CO) or pulmonary artery wedge pressure (PWP), but was slightly negatively correlated with mean arterial pressure (MAP) (r = -0.45) and systemic vascular resistance (SVR) (r = -0.40). After infusion of the angiotensin converting enzyme inhibitor teprotide (SQ 20,881) PWP fell from 26.3 ± 1.3 (SEM) to 20.3 ± 1.4 mm Hg (P < 0.001), CO rose from 3.94 ± 0.23 to 4.75 ± 0.31 1/min (P < 0.001), MAP fell from 87.5 ± 3.8 to 77.9 ± 4.1 mm Hg (P < 0.001) and SVR from 1619 ± 148 to 1252 ± 137 dyne-sec-cm-5 (P < 0.001). The fall in MAP and in SVR was significantly correlated with control PRA (r = 0.68 and r = 0.58, respectively). When subjects were divided on the basis of control PRA the hemodynamic response to teprotide was greatest in the high renin group. PRA rose after teprotide (8.7 ± 3.4 to 37.9 + 7.7 ng/ml/hr, P < 0.05) but plasma norepinephrine fell (619.1 ± 103.6 to 449.7 ± 75.7, P < 0.05). The renin-angiotensin system thus appears to have an important role in the elevated SVR in some patients with heart failure. Chronic inhibition of converting enzyme should be explored as a possible therapeutic approach.