Endocrinology of cardiac failure. Pathophysiologic aspects--hemodynamics.

S Persson
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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)

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心力衰竭的内分泌学。病理生理的方面——血液动力学。
充血性心力衰竭(CHF)的血流动力学状况受到心脏内部代偿机制以及中枢神经系统和肾脏释放的代偿机制的极大影响。这些措施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央循环和外周循环中。在心脏内部,肾上腺素能刺激引起心率和收缩力的增加,并在慢性过程中心肌肥厚也在起作用。中枢神经和外周适应性措施包括增加交感神经流出,增加血管舒缩张力,增加前负荷和后负荷,激活肾素-血管紧张素-醛固酮系统,其中血管紧张素II直接通过中枢神经刺激进一步增强血管收缩。这种血管收缩可被具有血管舒张特性的体液因子所抵消,如多巴胺、缓激肽、乙酰胆碱及其代谢产物腺苷和乳酸。它们的确切作用以及抗利尿激素、精氨酸抗利尿素、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。由于代偿机制可以在休息时维持相当满意的血流动力学状况,因此不仅在休息时进行调查,而且在运动时进行调查,以获得心脏功能状态的整体印象。(摘要删节250字)
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