Laffi G, Pinzani M, Meacci E, La Villa G, Renzi D, Baldi E, Cominelli F, Marra F, Gentilini P
Istituto di Clinica Medica II, University of Florence School of Medicine, Italy.
Gastroenterology. 1989 Jan;96(1):167-77. doi: 10.1016/0016-5085(89)90777-4.
We investigated the effect of a continuous infusion (50 micrograms as an initial bolus followed by a maintenance infusion at a rate of 0.1 micrograms/min.kg body wt for 45 min) of synthetic human atrial natriuretic factor (hANF) on renal hemodynamics and the renin-angiotensin-aldosterone system in 15 cirrhotic patients with ascites. Basal hANF levels were higher in cirrhotic patients when compared with normal values. Human atrial natriuretic factor infusion induced a significant decrease in mean blood pressure (from 77.8 +/- 1.1 to 68.6 +/- 1.5 mmHg, p less than 0.001) and a significant increase in heart rate (from 76.4 +/- 2.7 to 89.8 +/- 2.4 beats/min, p less than 0.001) in the patients studied. A remarkable increase in natriuresis (i.e., greater than or equal to 200 muEq/min) was observed in 5 patients (responders), whereas the infusion did not modify sodium excretion (i.e., less than or equal to 20 muEq/min) in 6 patients (nonresponders) and induced an intermediate response in 4 patients. Human atrial natriuretic factor-induced natriuresis was related to changes in renal hemodynamics that occurred during hANF infusion. In responders, the extent of the natriuretic response paralleled the increase of effective renal plasma flow and glomerular filtration rate; in non-responders the absent natriuretic response was associated with an evident reduction of these parameters. The reduction of blood pressure was similar in responders and nonresponders, but in the latter group it was followed by a marked increase of plasma renin activity and heart rate. It is likely that in nonresponders the natriuretic effect of hANF was blunted by the hemodynamic and hormonal changes triggered by the concomitant hANF-induced hypotension. This probably occurs in the presence of a greater reduction of effective arterial blood volume, as suggested by the higher baseline levels of plasma renin activity and the inability to increase free water excretion after a water load observed in nonresponders.
我们研究了持续输注合成人心房利钠因子（hANF）（初始推注50微克，随后以0.1微克/分钟·千克体重的速率维持输注45分钟）对15例肝硬化腹水患者肾血流动力学及肾素 - 血管紧张素 - 醛固酮系统的影响。与正常数值相比，肝硬化患者的基础hANF水平更高。在接受研究的患者中，输注人心房利钠因子导致平均血压显著降低（从77.8±1.1降至68.6±1.5 mmHg，p<0.001），心率显著增加（从76.4±2.7增至89.8±2.4次/分钟，p<0.001）。5例患者（反应者）出现显著的利钠增加（即≥200微当量/分钟），而6例患者（无反应者）输注后钠排泄未改变（即≤20微当量/分钟），4例患者出现中间反应。人心房利钠因子诱导的利钠作用与hANF输注期间发生的肾血流动力学变化有关。在反应者中，利钠反应的程度与有效肾血浆流量和肾小球滤过率的增加平行；在无反应者中，缺乏利钠反应与这些参数的明显降低相关。反应者和无反应者的血压降低相似，但在后者组中，血压降低后血浆肾素活性和心率显著增加。在无反应者中，hANF的利钠作用可能因伴随的hANF诱导的低血压引发的血流动力学和激素变化而减弱。这可能发生在有效动脉血容量降低更大的情况下，无反应者中较高的血浆肾素活性基线水平以及水负荷后无法增加自由水排泄提示了这一点。
