L-精氨酸可降低重度充血性心力衰竭患者的心率并改善血流动力学。
L-arginine reduces heart rate and improves hemodynamics in severe congestive heart failure.
作者信息
Bocchi E A, Vilella de Moraes A V, Esteves-Filho A, Bacal F, Auler J O, Carmona M J, Bellotti G, Ramires A F
机构信息
Heart Institute, Medical School of São Paulo University, Brazil.
出版信息
Clin Cardiol. 2000 Mar;23(3):205-10. doi: 10.1002/clc.4960230314.
BACKGROUND
Stimulated endothelium-derived relaxing factor-mediated vasodilation and conduit artery distensibility are impaired in congestive heart failure (CHF). L-arginine could have a potentially beneficial role in CHF, acting through the nitric oxide (NO)-L-arginine pathway or by growth hormone increment.
HYPOTHESIS
This study was undertaken to investigate the effects of L-arginine on heart rate, hemodynamics, and left ventricular (LV) function in CHF.
METHODS
In seven patients (aged 39 +/- 8 years) with CHF, we obtained the following parameters using echocardiography and an LV Millar Mikro-Tip catheter simultaneously under four conditions: basal, during NO inhalation (40 ppm), in basal condition before L-arginine infusion, and after L-arginine intravenous infusion (mean dose 30.4 +/- 1.9 g).
RESULTS
Nitric oxide inhalation increased pulmonary capillary wedge pressure from 25 +/- 9 to 31 +/- 7 mmHg (p < 0.05), but did not change echocardiographic variables or LV contractility by elastance determination. L-arginine decreased heart rate (from 88 +/- 15 to 80 +/- 16 beats/min, p<0.005), mean systemic arterial pressure (from 84 +/- 17 to 70 +/- 18 mmHg, p < 0.007), and systemic vascular resistance (from 24 +/- 8 to 15 +/- 6 Wood units, p<0.003). L-arginine increased right atrial pressure (from 7 +/- 2 to 10 +/- 3 mmHg, p<0.04), cardiac output (from 3.4 +/- 0.7 to 4.1 +/- 0.8 l/min, p < 0.009), and stroke volume (from 40 +/- 9 to 54 +/- 14 ml, p < 0.008). The ratios of pulmonary vascular resistance to systemic vascular resistance at baseline and during NO inhalation were 0.09 and 0.075, respectively, and with L-arginine this increased from 0.09 to 0.12.
CONCLUSION
L-arginine exerted no effect on contractility; however, by acting on systemic vascular resistance it improved cardiac performance. L-arginine showed a negative chronotropic effect. The possible beneficial effect of L-arginine on reversing endothelial dysfunction in CHF without changing LV contractility should be the subject of further investigations.
背景
在充血性心力衰竭（CHF）中，刺激的内皮衍生舒张因子介导的血管舒张和传导动脉扩张性受损。L-精氨酸可能通过一氧化氮（NO）-L-精氨酸途径或通过生长激素增加在CHF中发挥潜在的有益作用。
假设
本研究旨在探讨L-精氨酸对CHF患者心率、血流动力学和左心室（LV）功能的影响。
方法
在7例（年龄39±8岁）CHF患者中，我们在以下四种情况下同时使用超声心动图和LV Millar Mikro-Tip导管获取以下参数：基础状态、吸入NO期间（40 ppm）、L-精氨酸输注前的基础状态以及L-精氨酸静脉输注后（平均剂量30.4±1.9 g）。
结果
吸入一氧化氮使肺毛细血管楔压从25±9 mmHg升高至31±7 mmHg（p<0.05），但通过弹性测定未改变超声心动图变量或LV收缩性。L-精氨酸降低了心率（从88±15次/分钟降至80±16次/分钟，p<0.005）、平均体动脉压（从84±17 mmHg降至70±18 mmHg，p<0.007）和全身血管阻力（从24±8 Wood单位降至15±6 Wood单位，p<0.003）。L-精氨酸增加了右心房压力（从7±2 mmHg升至10±3 mmHg，p<0.04）、心输出量（从3.4±0.7升/分钟升至4.1±0.8升/分钟，p<0.009）和每搏输出量（从40±9 ml升至54±14 ml，p<0.008）。基线时和吸入NO期间肺血管阻力与全身血管阻力的比值分别为0.09和0.075，使用L-精氨酸后该比值从0.09增加至0.12。
结论
L-精氨酸对收缩性无影响；然而，通过作用于全身血管阻力，它改善了心脏功能。L-精氨酸显示出负性变时作用。L-精氨酸在不改变LV收缩性的情况下对逆转CHF内皮功能障碍的可能有益作用应是进一步研究的主题。
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