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充血性心力衰竭的外周适应性:综述

Peripheral adaptations in congestive heart failure: a review.

作者信息

Just H

机构信息

Medizinische Universitätsklinik, Freiburg, Federal Republic of Germany.

出版信息

Am J Med. 1991 May 29;90(5B):23S-26S. doi: 10.1016/0002-9343(91)90269-4.

Abstract

In congestive heart failure, peripheral adaptive mechanisms play a significant and largely underestimated role. In acute heart failure, sympathetic-mediated peripheral vasoconstriction together with chronotropic and inotropic actions serves to maintain perfusion pressure and blood supply to the vital organs. In chronic heart failure, activation of the renin-angiotensin system increases peripheral vascular resistance and arterial tone and decreases arterial compliance and vasodilator capacity. Endothelium-mediated, flow-dependent vasodilation is reduced as a consequence of reduced blood flow. Deconditioning renders the blood vessels incapable of dilating in response to increased flow. Simultaneously, reduced blood flow and inactivity are induced by deconditioning, with functional and structural consequences within the skeletal muscle. Exercise performance is limited by reduced overall blood flow, reduced conductance of the feeding arteries, elevated tone of the resistance vessels, reduced vasodilator capacity, impaired dissipation of heat from the working muscle, and functional and structural changes of the skeletal muscle due to underperfusion and inactivity. The adaptive mechanisms operate at different time scales. Under therapeutic intervention, their reversibility also follows different time constants. Restoration of the vasodilator capacity of the large arteries and of the abnormalities of skeletal muscle in heart failure requires time. Vasodilation with reduced pre- and/or afterload will retard progression of the superimposed ventricular dilation and hypertrophy, and therefore retard the progress of the disease. However, restoration of the peripheral blood flow and of organ function will require time. Restoration of the vascular compliance and of the full amplitude of adaptive flow-dependent vasodilation in the large arteries requires weeks or months. Similarly, restoration of functionally and morphologically altered skeletal muscle can be expected to be reversible over a longer time period.

摘要

在充血性心力衰竭中,外周适应性机制发挥着重要且在很大程度上被低估的作用。在急性心力衰竭中,交感神经介导的外周血管收缩以及变时性和变力性作用有助于维持灌注压和重要器官的血液供应。在慢性心力衰竭中,肾素 - 血管紧张素系统的激活会增加外周血管阻力和动脉张力,并降低动脉顺应性和血管舒张能力。由于血流减少,内皮介导的、血流依赖性血管舒张会减弱。失健使得血管无法对增加的血流做出扩张反应。同时,失健会导致血流减少和活动减少,从而对骨骼肌产生功能和结构上的影响。运动能力受限是由于整体血流减少、供血动脉传导性降低、阻力血管张力升高、血管舒张能力降低、工作肌肉散热受损以及由于灌注不足和活动减少导致的骨骼肌功能和结构变化。这些适应性机制在不同的时间尺度上起作用。在治疗干预下,它们的可逆性也遵循不同的时间常数。恢复心力衰竭患者大动脉的血管舒张能力和骨骼肌异常需要时间。降低前负荷和/或后负荷的血管舒张将延缓叠加的心室扩张和肥厚的进展,从而延缓疾病的进程。然而,恢复外周血流和器官功能需要时间。恢复大动脉的血管顺应性和适应性血流依赖性血管舒张的全幅度需要数周或数月。同样,功能和形态改变的骨骼肌的恢复预计在更长的时间段内是可逆的。

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