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心力衰竭的内分泌学。病理生理方面——血流动力学

Endocrinology of cardiac failure. Pathophysiologic aspects--hemodynamics.

作者信息

Persson S

出版信息

Acta Med Scand Suppl. 1986;707:7-14.

PMID:2943144
Abstract

The hemodynamic situation in congestive heart failure (CHF) is greatly influenced by compensatory mechanisms within the heart itself as well as released from the central nervous system and from the kidneys. These measures are intended to maintain the cardiac output at a level as beneficial as possible and to distribute the blood flow to regions with the largest metabolic demands. Thus the hemodynamic consequences of CHF are reflected in the central circulation as well as in the periphery. Within the heart the Frank-Starling mechanism, adrenergic stimulation causing increase of heart rate and contractility, and during the chronic course also myocardial hypertrophy are operating. The central nervous and peripheral adaptive measures include increased sympathetic outflow bringing about an increased vasomotor tone with augmentation of pre- and afterload, and activation of the renin-angiotensin-aldosterone system, where angiotensin II further augments vasoconstriction directly and through central nervous stimulation. This vasoconstriction may be counteracted by humoral factors with vasodilatory properties, such as dopamine, bradykinin, acetylcholine and the metabolic products adenosine and lactic acid. The exact role of these and the possible importance of the antidiuretic hormone, arginine vasopressin, the prostaglandin system and the recently discovered atriopeptin remains to be established. As the compensatory mechanisms may maintain a fairly satisfactory hemodynamic situation at rest, investigations should be performed not only at rest but also during exercise to get an over-all impression of the cardiac functional state.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

充血性心力衰竭(CHF)的血流动力学状况受到心脏自身以及中枢神经系统和肾脏释放的代偿机制的极大影响。这些机制旨在将心输出量维持在尽可能有益的水平,并将血流分配到代谢需求最大的区域。因此,CHF的血流动力学后果反映在中心循环和外周循环中。在心脏内部,Frank-Starling机制、导致心率和收缩力增加的肾上腺素能刺激以及在慢性病程中还包括心肌肥大都在起作用。中枢神经和外周适应性措施包括交感神经输出增加,导致血管运动张力增加,前负荷和后负荷增大,以及肾素-血管紧张素-醛固酮系统的激活,其中血管紧张素II通过直接作用和中枢神经刺激进一步增强血管收缩。这种血管收缩可能会被具有血管舒张特性的体液因子抵消,如多巴胺、缓激肽、乙酰胆碱以及代谢产物腺苷和乳酸。这些因子的确切作用以及抗利尿激素、精氨酸加压素、前列腺素系统和最近发现的心房肽的可能重要性仍有待确定。由于代偿机制可能在静息状态下维持相当令人满意的血流动力学状况,因此不仅应在静息状态下进行研究,还应在运动期间进行研究,以全面了解心脏功能状态。(摘要截断于250字)

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