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[心力衰竭的神经激素评估:从精密实验室到实际应用指征]

[Neurohormonal assessment in heart failure: from the sophisticated laboratory to practical indications].

作者信息

Dei Cas L, Metra M, Visioli O

机构信息

Cattedra di Cardiologia, Università degli Studi di Brescia.

出版信息

G Ital Cardiol. 1993 Feb;23(2):193-204.

PMID:8098306
Abstract

Heart failure is a syndrome characterized by the activation of neurohumoral mechanisms (sympathoadrenergic, renin-angiotensin, vasopressin) which cause peripheral vasoconstriction, sodium retention and myocardial hypertrophy. In acute myocardial disfunction these systems can play a critical role in patient survival, however, they can directly worsen myocardial function and patient prognosis on a long-term basis. Other neurohumoral systems activated in heart failure (atrial natriuretic factor, prostaglandins, dopamine) tend to counterbalance the vasoconstrictive, sodium retentive mechanisms. Though their secretion is increased in heart failure, it is however not sufficient, and peripheral vasoconstriction and sodium retention prevail. Moreover the role of local factors, such as tissue renin-angiotensin system, EDRF and endothelin secretion has been recently pointed out. Neurohumoral activation is directly related to the severity of the clinical and hemodynamic impairment and prognosis of the patient with heart failure. A thorough evaluation of the neurohumoral mechanisms is therefore of paramount importance for the assessment of patients with heart failure. Neurohumoral activation can be roughly assessed using some simple laboratory measurements: plasma sodium concentration, for example, is inversely related to the degree of activation of many neurohormones such as norepinephrine, angiotensin II, vasopressin and atrial natriuretic factor. The method most commonly used to assess neurohumoral activity relies on the direct measurement of the plasma concentrations. It must be noted, however, that plasma levels are critically dependent on many factors besides hormone secretion and metabolism. For example, 3-4 days on a low sodium diet or standing for at least 2 hours can increase plasma renin activity in a normal subject from 1.5 to 5-10 pg/ml/hr. Plasma concentrations of neurohormones are related to the factors controlling their secretion: for example, "normal" values of plasma renin activity in presence of fluid retention and edema are to be judged as excessively elevated. Autonomic nervous system activity can also be assessed studying reflexes in which this system is involved (orthostasis, cold pressor test, phenylephrine test...). Another method consists in the study of the spontaneous variability of some parameters controlled by this system, such as heart rate and blood pressure. The most reliable method is based on the power spectral analysis of heart rate variability. With this last method, a low frequency component depending mainly on sympathetic activity and an high frequency component depending on vagal activity can be identified in heart rate variability. Thus, complex phenomena such as sympatho-vagal balance can be easily studied through simple noninvasive tools.

摘要

心力衰竭是一种以神经体液机制(交感肾上腺素能、肾素 - 血管紧张素、血管加压素)激活为特征的综合征,这些机制会导致外周血管收缩、钠潴留和心肌肥厚。在急性心肌功能障碍时,这些系统对患者生存可能起关键作用,然而,从长期来看,它们会直接使心肌功能和患者预后恶化。心力衰竭时激活的其他神经体液系统(心房利钠因子、前列腺素、多巴胺)倾向于抵消血管收缩、钠潴留机制。尽管它们在心力衰竭时分泌增加,但并不足够,外周血管收缩和钠潴留仍占主导。此外,最近还指出了局部因素的作用,如组织肾素 - 血管紧张素系统、内皮舒张因子和内皮素分泌。神经体液激活与心力衰竭患者的临床和血流动力学损害严重程度及预后直接相关。因此,全面评估神经体液机制对心力衰竭患者的评估至关重要。神经体液激活可通过一些简单的实验室测量大致评估:例如,血浆钠浓度与许多神经激素如去甲肾上腺素、血管紧张素 II、血管加压素和心房利钠因子的激活程度呈负相关。评估神经体液活性最常用的方法依赖于直接测量血浆浓度。然而,必须注意的是,血浆水平除了取决于激素分泌和代谢外,还严重依赖许多其他因素。例如,正常受试者低钠饮食 3 - 4 天或站立至少 2 小时可使血浆肾素活性从 1.5 增加至 5 - 10 pg/ml/hr。神经激素的血浆浓度与控制其分泌的因素有关:例如,在存在液体潴留和水肿时,血浆肾素活性的“正常”值应被判定为过度升高。自主神经系统活性也可通过研究该系统参与的反射(直立位、冷加压试验、去氧肾上腺素试验等)来评估。另一种方法是研究该系统控制的一些参数的自发变异性,如心率和血压。最可靠的方法基于心率变异性的功率谱分析。通过最后这种方法,在心率变异性中可识别出主要依赖交感神经活动的低频成分和依赖迷走神经活动的高频成分。因此,诸如交感 - 迷走平衡等复杂现象可通过简单的非侵入性工具轻松研究。

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