Sustained improvement in flow-mediated vasodilation after short-term administration of dobutamine in patients with severe congestive heart failure.
Sustained improvement in flow-mediated vasodilation after short-term administration of dobutamine in patients with severe congestive heart failure.
复制标题
严重充血性心力衰竭患者短期给予多巴酚丁胺后血流介导的血管舒张持续改善。
作者：
Mrugesh B. Patel;I. Kaplan;R. Patni;Dan Levy;Joel A. Strom;Jamshid Shirani;T. LeJemtel
背景
在严重充血性心力衰竭（CHF）患者中，短期给予多巴酚丁胺可产生持续的临床获益，部分是通过对骨骼肌的训练样作用介导的。最近，体育训练已被证明可以通过改善内皮功能来增强骨骼肌血管系统中的内皮功能。多巴酚丁胺诱导的训练效应是否也与骨骼肌血管内皮功能的改善有关，目前尚不清楚。
方法和结果
对9例重度CHF患者前臂进行多巴酚丁胺治疗72小时，评价了反应性充血峰值时血流介导的血管舒张反应。在基线、多巴酚丁胺输注期间3小时和72小时以及停用多巴酚丁胺治疗后2周和4周，通过二维和多普勒超声测量静息和充血峰值肱动脉血流量和直径（分别为BABF [mL/min]和BAD [mm]）。此外，在基线和多巴酚丁胺治疗停止后2周和4周评价了舌下（SL）给予硝酸甘油（NTG）的肱动脉反应。10例未接受多巴酚丁胺治疗的重度CHF患者作为对照组。静息BABF在3小时和72小时时显著增加（分别为391.2+/-31.8和366.8+/-31.0 mL/min，而基线时为289.8+/-18.6 mL/min; P<0.05）。与基线值相比，多巴酚丁胺输注未改变充血性BABF峰值。输注多巴酚丁胺72小时后，充血反应高峰期BAD的增加更大（15.2+/-2.7%vs9.1 +/-1.8%，P <0.05），停用多巴酚丁胺2周后，BAD的增加仍显著更大（12.3+/-2.2%vs9.1 +/-1.8%，P <0.05）。与充血反应峰值相反，多巴酚丁胺给药72小时后，SL NTG诱导的BAD（%）增加无变化。多巴酚丁胺停药后2周和4周，NTG诱导的BAD增加与基线时观察到的BAD相似。
结论
在重度CHF患者中，短期给予多巴酚丁胺72小时选择性改善血管内皮功能≥ 2周。
BACKGROUND
In patients with severe congestive heart failure (CHF), short-term administration of dobutamine exerts sustained clinical benefits that are partially mediated by a training-like effect on skeletal muscle. Recently, physical training has been shown to enhance endothelial function in the skeletal muscle vasculature by improving endothelial function. Whether the dobutamine-induced training effect is also associated with an improvement in endothelial function in the skeletal muscle vasculature is currently unknown.
METHODS AND RESULTS
Flow-mediated vasodilation in response to peak reactive hyperemia was evaluated in the forearms of 9 patients with severe CHF who were treated with dobutamine for 72 hours. Resting and peak hyperemic brachial artery blood flow and diameter (BABF [mL/min] and BAD [mm], respectively) were measured by 2-dimensional and Doppler ultrasonography at baseline, at 3 and 72 hours during dobutamine infusion, and at 2 and 4 weeks after discontinuation of dobutamine therapy. In addition, the brachial artery response to sublingual (SL) administration of nitroglycerin (NTG) was evaluated at baseline and at 2 and 4 weeks after discontinuation of dobutamine therapy. Ten patients with severe CHF who did not receive dobutamine served as control subjects. Resting BABF was significantly increased at 3 and 72 hours (391.2+/-31.8 and 366.8+/-31.0 mL/min, respectively, compared with 289.8+/-18.6 mL/min at baseline; P<0.05). Peak hyperemic BABF was not altered by dobutamine infusion compared with baseline values. The increase in BAD during peak hyperemic response was greater after infusion of dobutamine for 72 hours (15.2+/-2.7% versus 9.1+/-1.8%, P<0.05) and remained significantly greater for >/=2 weeks after discontinuation of dobutamine (12.3+/-2.2% versus 9.1+/-1.8%, P<0.05). In contrast to the peak hyperemic response, the increase in BAD (%) induced by SL NTG was unchanged by administration of dobutamine for 72 hours. Two and 4 weeks after discontinuation of dobutamine, NTG-induced increases in BAD were similar to the BAD noted at baseline.
CONCLUSIONS
In patients with severe CHF, short-term administration of dobutamine for 72 hours selectively improves vascular endothelial function for >/=2 weeks.