Ultrafiltration should not replace diuretics for the initial treatment of acute decompensated heart failure.
Ultrafiltration should not replace diuretics for the initial treatment of acute decompensated heart failure.
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DOI：
10.1161/circheartfailure.109.862474
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发表时间：
2009-09
期刊：
影响因子：
--
通讯作者：
Dec GW
中科院分区：
文献类型：
--
作者：
Shin JT;Dec GW
钠潴留对血管功能和高血压的发病机制有着深远的影响。9过量钠抑制动脉和小动脉血管平滑肌细胞的Na泵/Na-K-ATP酶，刺激钠-钙交换。这导致细胞内钙水平升高和血管收缩。10此外，钠潴留会减少一氧化氮的合成，并增加不对称二甲基L-精氨酸（一氧化氮产生的内源性抑制剂）的水平。11钠潴留也会导致强制性（被动）水蓄积，最终导致细胞外液量增加和左右侧压力增加。左侧血压升高导致肺充血，临床表现为劳力性呼吸困难、端坐呼吸、咳嗽、咯血、罗音和特征性X线表现。高的左侧压力还引起左心室腔室扩张和二尖瓣环的变形，通常导致二尖瓣瓣叶的接合不良和显著的二尖瓣返流。12左心室腔扩张增加了室壁张力和心肌需氧量，达到可能发生心肌缺血和/或坏死的程度。功能性二尖瓣返流和心肌缺血或坏死对心输出量产生不利影响，最终导致症状恶化、交感神经和RAAS系统进一步激活、钠潴留增加和心脏重塑加速（图1）。7
Sodium retention has a profound effect on vascular function and the pathogenesis of hypertension. 9 Excess sodium inhibits the Na pump/Na-K-ATPase of arterial and arteriolar vascular smooth muscle cells stimulating the sodium-calcium exchanger. This leads to increased intracellular calcium levels and vasoconstriction. 10 In addition, sodium retention decreases the synthesis of nitric oxide and increases levels of asymmetrical dimethl L-arginine, an endogenous inhibitor of nitric oxide production. 11Sodium retention also causes obligatory (passive) water accumulation that ultimately leads to increased extracellular fluid volume and increased left and right-sided pressures. 1, 7 Elevated left-sided pressures result in pulmonary congestion, which is recognized clinically by dyspnea on exertion, orthopnea, cough, hemoptysis, rales, and characteristic radiographic findings. High left-sided pressures also cause left ventricular chamber dilation and distortion of the mitral annulus often leading to malcoaptation of the mitral valve leaflets and significant mitral regurgitation. 12 Left ventricular chamber dilation increases wall tension and myocardial oxygen demand to the extent that myocardial ischemia and/or necrosis may occur. Functional mitral regurgitation and myocardial ischemia or necrosis adversely affect cardiac output ultimately leading to worsening symptoms, further activation of the sympathetic and RAAS systems, increased sodium retention and acceleration of cardiac remodeling (Figure 1). 7