Augmented Sympathetic Neurotransmitter Activity in the Peripheral Vascular Bed of Patients with Congestive Heart Failure and Cardiac Norepinephrine Depletion
Augmented Sympathetic Neurotransmitter Activity in the Peripheral Vascular Bed of Patients with Congestive Heart Failure and Cardiac Norepinephrine Depletion
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充血性心力衰竭和心脏去甲肾上腺素耗竭患者外周血管床交感神经递质活性增强
DOI：
10.1161/01.cir.38.4.629
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发表时间：
1968
期刊：
影响因子：
37.8
通讯作者：
E. Braunwald
中科院分区：
文献类型：
--
作者：
R. S. Kramer;D. Mason;E. Braunwald
由于充血性心力衰竭患者的交感神经活动总体增强，而肾上腺髓质功能正常且心脏中的神经递质储备减少，因此研究针对外周血管床中肾上腺素能受体的功能状态和可用的去甲肾上腺素储备。将八名充血性心力衰竭患者动脉内注射酪胺和去甲肾上腺素后，通过体积描记法确定的血流量和计算出的小腿血管阻力与九名患有心脏病但无心力衰竭的患者的反应进行比较。在心力衰竭患者中，分级剂量的去甲肾上腺素产生的血管阻力的绝对增加更大。然而，任何剂量的去甲肾上腺素产生的血管阻力的相对增强在两组中基本相同。相比之下，在心力衰竭的情况下，对标准剂量的间接作用拟交感神经药酪胺的血管收缩反应显着增强（P<0.01），无论是根据血管阻力的相对上升还是根据产生类似阻力升高所需的注射去甲肾上腺素的量来考虑这种增加的反应。药理学研究完成几天后进行心脏手术时测定的心房组织中去甲肾上腺素的浓度在心力衰竭患者中显着降低。结论是，小腿外周小动脉床神经末梢可被酪胺释放的内源性交感神经递质的数量并没有减少，甚至在心力衰竭患者中可能会增加，心力衰竭状态下血浆去甲肾上腺素水平升高至少部分源自外周血管床中不稳定的肾上腺素能储备。
Since there is an overall augmentation of sympathetic nervous activity in patients with congestive heart failure while adrenal medullary function is normal and neurotransmitter stores are diminished in the heart, investigation was directed to the functional status of adrenergic receptors and available norepinephrine stores in the peripheral vascular beds. Blood flow, determined plethysmographically, and vascular resistance, calculated in the calf, following intra-arterial injections of tyramine and norepinephrine in eight patients with congestive heart failure were compared to the responses in nine patients with heart disease but without heart failure. The absolute increase in vascular resistance produced by graded doses of norepinephrine was greater in patients with heart failure. However, the relative augmentation of vascular resistance produced by any dose of norepinephrine was essentially identical in the two groups. In contrast, the vasoconstrictor response to a standard dose of the indirectly acting sympathomimetic agent, tyramine, was markedly enhanced (P<0.01) in cases of heart failure, both when this increased response was considered in terms of the relative rise in vascular resistance, and in the quantity of injected norepinephrine required to produce a similar elevation of resistance. Concentration of norepinephrine in atrial tissue, determined at the time of cardiac surgery a few days after completion of the pharmacological studies, was significantly lower in the patients with heart failure. It is concluded that the quantity of endogenous sympathetic neurotransmitter available for release by tyramine from nerve endings in the peripheral arteriolar bed in the calf is not reduced and may even be augmented in patients with heart failure, and that the elevated levels of plasma norepinephrine in the heart failure state are derived, at least in part, from labile adrenergic stores in the peripheral vascular bed.