With Cardiac Disease with Special Emphasis on -ANP Clinical Significant of Atrial Natriuretic Peoptide in Patients

正常人循环心钠素(ANP)主要由α-型心钠素组成。心力衰竭患者的血浆心钠素水平升高，而心力衰竭患者的血浆心钠素水平与心力衰竭患者的血浆心钠素水平相关。然而，心力衰竭患者中ANP的循环形式仍不清楚。为探讨心钠素在心力衰竭中的临床意义，我们采用凝胶过滤和反相高效液相色谱法分析了慢性心力衰竭患者血浆心钠素的分子形态。随着心力衰竭的进展，血浆中β-型心钠素占总心钠素的比例逐渐增加，同时也出现了伽玛型心钠素。在成功治疗心力衰竭后，循环中的β-形式相反地下降。在体外循环心脏手术中，血浆ANP水平在全主动脉阻断(TACC)后无明显下降，在TACC释放后显著升高，且以α形式为主，无明显的β或γ形式。在慢性肾功能衰竭患者中，主要的循环ANP是α-型，尽管在某些情况下也存在β-型。血液透析后，血浆ANP水平下降，主要是α-型，提示：1)心功能不全大鼠心钠素的生物合成活性增强与从α-型到α-型和β-型的过程增加有关；2)由于心房压力的即刻升高，ATCC释放后ANP的分泌过程与正常人基本相似；3)一些肾功能衰竭患者循环β型的出现可能是由于代谢延迟、体液增加或心肌代谢改变所致，但其病理生理功能尚不清楚。从我们的结果看，循环中的β-ANP应该是一个有用的标记物，作为评估心力衰竭及其治疗结果的无创性参数。

Circulating atrial natriuretic peptide (ANP) consists predominantly of alpha-form in normal subjects. Plasma ANP levels are elevated in patients with heart failure, which increase in relation to its seventy. However, circulating forms of ANP in patients with heart failure remain unknown. To elucidate clinical significance of ANP in heart failure, we have analyzed the molecular forms of plasma ANP in patients with conjestive heart failure by gel filtration and reverse-phase HPLC. As the seventy of heart failure progressed, the proportion of beta-form to the total ANP in plasma increased, and gamma-form also appeared. Circulating beta-form conversely decreased after successful treatment for heart failure. During cardiac surgery with extracorporeal circulation, plasma ANP levels did not significantly decrease after total aortic cross claming (TACC), remarkably increased after the release of TACC, where alpha-form predominated without distinct beta- or gamma-form. In patients with chronic renal failure, the predominant circulating ANP was alpha-form, although beta-form was also present in some cases. After hemodialysis, plasma ANP levels, mostly alpha-form, decreased these rats suggest that 1) the enhanced biosynthetic activity of ANP in the faility heart is associated with the increased processing from gamma- to alpha- and beta-form, 2) the processing of ANP secreted after the release of ATCC due to immediate rise in atrial pressure appears to be essentially similar to that of normal subjects, 3) the appearance of circulating beta-form in some renal failure patients may be due to delayed metabolism, increased body fluid and or metabolic change of myocardium, although its pathophysislogical function remains undetermined. From our results it appears that circulating beta-ANP should be a useful marker as a noninvasive parameter for assessment of heart failure as well as its therapeutic outcome.