Rouleau J L, Bichet D, Kortas C
Centre de Recherche, Hôpital du Sacré-Coeur de Montréal, Quebec, Canada.
Am Heart J. 1988 May;115(5):1060-7. doi: 10.1016/0002-8703(88)90077-4.
The response of atrial natriuretic peptide (ANP) to standing and the acute and chronic administration of the vasodilator, captopril, were examined in 15 patients with chronic congestive heart failure. In the supine position, ANP was increased (361 +/- 202 pg/ml); however, only a loose correlation existed between atrial pressures and ANP (right atrial vs ANP, r = 0.03, p = N.S., and pulmonary capillary wedge pressures vs ANP, r = 0.4, p = N.S.). Standing and acute captopril therapy decreased atrial pressures and ANP but did not significantly improve the correlation between atrial pressures and ANP. With chronic captopril therapy, atrial pressures remained decreased; however, ANP had returned to control values (370 +/- 254 pg/ml vs 361 +/- 202 pg/ml) and failed to decrease with standing (370 +/- 259 pg/ml lying vs 351 +/- 194 pg/ml standing). These changes in ANP (with chronic captopril therapy) persisted even once the hemodynamic effects of captopril had dissipated (3 hours post dose). This study indicates that in patients with severe chronic congestive heart failure (1) only a poor correlation exists between ANP and atrial pressures and (2) with chronic captopril therapy ANP increases to higher levels for a given atrial pressure and fails to decrease with standing despite a decrease in atrial pressures.
对15例慢性充血性心力衰竭患者,研究了心房利钠肽(ANP)对站立及急性和慢性给予血管扩张剂卡托普利的反应。在仰卧位时,ANP升高(361±202 pg/ml);然而,心房压力与ANP之间仅存在微弱相关性(右心房压力与ANP,r = 0.03,p =无显著性差异,肺毛细血管楔压与ANP,r = 0.4,p =无显著性差异)。站立和急性卡托普利治疗可降低心房压力和ANP,但并未显著改善心房压力与ANP之间的相关性。慢性卡托普利治疗后,心房压力仍降低;然而,ANP已恢复至对照值(370±254 pg/ml对361±202 pg/ml),且站立时未降低(卧位时370±259 pg/ml对站立时351±194 pg/ml)。即使卡托普利的血流动力学效应已消失(给药后3小时),这些ANP的变化(慢性卡托普利治疗后)仍持续存在。本研究表明,在重度慢性充血性心力衰竭患者中,(1)ANP与心房压力之间仅存在较差的相关性;(2)慢性卡托普利治疗后,在给定的心房压力下ANP升高至更高水平,尽管心房压力降低,但站立时ANP并未降低。