The effects of bromocriptine in patients with congestive heart failure.
The effects of bromocriptine in patients with congestive heart failure.
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DOI：
10.1016/0002-8703(83)90446-5
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发表时间：
1983-07
影响因子：
4.8
通讯作者：
G. Francis;R. Parks;J. Cohn
中科院分区：
文献类型：
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作者：
G. Francis;R. Parks;J. Cohn
充血性心力衰竭（CHF）患者交感神经系统和肾素-血管紧张素系统被激活，可能导致周围血管过度收缩和心肌功能受损。溴隐肽是一种口服活性麦角生物碱，具有多巴胺能受体激动作用，已知可降低人血浆去甲肾上腺素。它也可能通过血管多巴胺能受体具有直接的血管扩张活性。为了评估溴隐汀对心力衰竭患者血液动力学测量、交感神经系统活动和肾素-血管紧张素系统的影响，我们测量了10例慢性稳定型心力衰竭患者口服单剂量2.5 mg溴隐汀前后的标准血液动力学参数、血浆去甲肾上腺素和血浆肾素活性。血浆去甲肾上腺素从581±194的平均±1 SD降至366±181 pg/ml；平均心率由87±16 bpm降至78±17 bpm；平均血压由87±9降至73±9 mmhg；全身血管阻力从1494±361下降到1249±289达因·SEC·cm−5；卒中容积指数由27±7 ml/beat/M2增加到33±10 ml/ M2；左室充盈压由28±8 mm Hg降至21±8 mm Hg；平均右房压由10±4 mm Hg降至7±4 mm Hg，血浆肾素活性无明显变化。所有病人对这种药的耐受性都很好。虽然溴隐亭对血浆去甲肾上腺素的影响可能有助于改善血液动力学状态，但其他作用机制也可能起作用。通过刺激血管多巴胺能受体直接产生血管舒张效应是可能的。我们得出结论，溴隐亭可改善心力衰竭患者的血流动力学特征，长期研究可以更好地描述该药物的作用。
The sympathetic nervous system and the renin-angiotensin system are activated in patients with congestive heart fallure (CHF) and could be contributing to excessive peripheral vasoconstriction and impaired myocardial performance. Bromocriptine, an orally active ergot alkaloid with dopaminergic receptor agonist actions, is known to lower plasma norepinephrine in humans. It could also possess direct vasodilator activity through vascular dopaminergic receptors. To assess the effects of bromocriptine on hemodynamic measurements, sympathetic nervous system activity, and the renin-angiotensin system in patients with heart failure, we measured standard hemodynamic parameters and plasma norepinephrine and plasma renin activity before and following a single oral dose of 2.5 mg of bromocriptine in 10 patients with chronic stable heart failure. The following statistically significant (p< 0.01) peak responses were noted: plasma norepinephrine decreased from a mean ± 1 SD of 581 ± 194 to 366 ± 181 pg/ml; mean heart rate declined from 87 ± 16 to 78 ± 17 bpm; mean blood pressure was reduced from 87 ± 9 to 73 ± 9 mm Hg; systemic vascular resistance decreased from 1494 ± 361 to 1249 ± 289 dynes · sec · cm−5; stroke volume index increased from 27 ± 7 to 33 ± 10 ml/beat/M2; left ventricular filling pressure decreased from 28 ± 8 to 21 ± 8 mm Hg; and mean right atrial pressure fell from 10 ± 4 to 7 ± 4 mm Hg. Plasma renin activity did not change significantly. All patients tolerated the drug well. Although the effects of bromocriptine on plasma norepinephrine may contribute to an improved hemodynamic state, other mechanisms of action are likely. A direct vasodilator effect via vascular dopaminergic receptor stimulation is possible. We conclude that bromocriptine improves the hemodynamic profile in heart failure acutely and that long-term studies are appropriate to better characterize the role of this agent.