Drexler H, Finkh M, Höing S, Toth M, Just H, Lang R E
Medizinische Klinik III, University of Freiburg, F.R.G.
Basic Res Cardiol. 1987 Nov-Dec;82(6):517-29. doi: 10.1007/BF01907221.
To characterize the systemic and regional vascular effects of atrial natriuretic peptide (ANP) in chronic heart failure, central hemodynamics, regional blood flow and plasma ANP levels were determined in a rat model of myocardial infarction and failure and in sham-operated animals. Measurements were made in the conscious state before and after intravenous rANP [99-126] (8 micrograms bolus followed by continuous infusion of 1.0 microgram/kg/min). With this protocol, ANP significantly decreased cardiac output, right atrial, left ventricular end-diastolic and arterial pressures and there were increases in heart rate, systemic and intestinal vascular resistances in sham animals. Renal blood flow per gram of tissue was unchanged with ANP, but when expressed as a percentage of cardiac output, increased significantly, indicating a preferential renal vasodilatory effect of ANP. In rats with infarction and failure, this dose did not alter cardiac output or arterial pressure, but decreased right atrial and left ventricular blood flow. Although significantly reduced as compared to the control group, renal blood flow was not improved with ANP in the heart failure group. ANP plasma levels of the heart failure group were elevated at baseline (p less than 0.01), and increased 5-10 times after infusion of rANP. Thus, in rats with chronic heart failure, the renal vascular effects of ANP are blunted, which may, in part, explain the failure of ANP to restore the altered volume homeostasis in heart failure despite elevated ANP plasma levels. However, the effects on venous return were preserved which, in turn, improved cardiac performance via a reduction of preload.
为了阐明心房利钠肽（ANP）在慢性心力衰竭中的全身和局部血管效应，我们在心肌梗死和心力衰竭大鼠模型以及假手术动物中测定了中心血流动力学、局部血流量和血浆ANP水平。在静脉注射重组ANP[99 - 126]（8微克推注，随后以1.0微克/千克/分钟持续输注）前后的清醒状态下进行测量。按照此方案，ANP显著降低了假手术动物的心输出量、右心房、左心室舒张末期和动脉压，同时心率、全身和肠道血管阻力增加。每克组织的肾血流量在使用ANP后未发生变化，但以心输出量的百分比表示时则显著增加，表明ANP具有优先的肾血管舒张作用。在梗死和心力衰竭大鼠中，该剂量未改变心输出量或动脉压，但降低了右心房和左心室血流量。虽然与对照组相比显著降低，但心力衰竭组使用ANP后肾血流量并未改善。心力衰竭组的ANP血浆水平在基线时升高（p < 0.01），在输注重组ANP后增加了5 - 10倍。因此，在慢性心力衰竭大鼠中，ANP的肾血管效应减弱，这可能部分解释了尽管ANP血浆水平升高，但ANP仍无法恢复心力衰竭时改变的容量稳态的原因。然而，对静脉回流的作用得以保留，进而通过降低前负荷改善了心脏功能。
