Burger Andrew J
Beth Israel Deaconess Medical Center, Noninvasive Cardiology Laboratory, Baker-3, 1 Deaconess Road, Boston, MA 02215, USA.
Congest Heart Fail. 2005 Jan-Feb;11(1):30-8. doi: 10.1111/j.1527-5299.2005.03794.x.
Adverse neurohormonal activation is an essential component in the pathogenesis of acute decompensated congestive heart failure (CHF). Consequently, blunting this activation is an important therapeutic goal. B-type natriuretic peptide (BNP) is a counterregulatory hormone produced by the ventricles in response to pressure and volume load. Endogenous BNP levels are significantly elevated in patients with acute CHF, but these levels are frequently inadequate to overcome the excess neurohormonal activation present in this condition. Infusion of nesiritide, a recombinant form of endogenous human BNP, increases circulating BNP levels by several-fold, augmenting the counterregulatory effects of this hormone. Clinical trials demonstrate that in patients with acute decompensated CHF, nesiritide produces arterial and venous vasodilation, reducing both preload and afterload; blunts adverse neurohormones, including renin, aldosterone, norepinephrine, and endothelin-1; and improves renal hemodynamics and tubular function. As a result, nesiritide quickly reduces clinical symptoms and improves mortality in patients with acute CHF.
不良神经激素激活是急性失代偿性充血性心力衰竭（CHF）发病机制中的一个重要组成部分。因此，抑制这种激活是一个重要的治疗目标。B型利钠肽（BNP）是心室在压力和容量负荷作用下产生的一种反调节激素。急性CHF患者的内源性BNP水平显著升高，但这些水平往往不足以克服该病症中存在的过度神经激素激活。输注奈西立肽（一种内源性人BNP的重组形式）可使循环BNP水平升高数倍，增强该激素的反调节作用。临床试验表明，在急性失代偿性CHF患者中，奈西立肽可引起动脉和静脉血管舒张，降低前负荷和后负荷；抑制包括肾素、醛固酮、去甲肾上腺素和内皮素-1在内的不良神经激素；并改善肾血流动力学和肾小管功能。因此，奈西立肽可迅速减轻急性CHF患者的临床症状并改善其死亡率。
