Feldman R C, Ball R M, Winchester M A, Jaillon P, Kates R E, Harrison D C
Am Heart J. 1981 May;101(5):534-40. doi: 10.1016/0002-8703(81)90218-0.
Thirteen patients with advanced congestive heart failure (CHF) were treated with prazosin. Following the first dose, cardiac output (CO) (mean +/- SD) rose from 3.2 +/- 1.2 to 4.3 +/- 1.1 L/min, pulmonary artery diastolic pressure (PAD) decreased from 23 +/- 12 to 18 +/- 11 mm Hg, mean arterial pressure (MAP) decreased from 85 +/- 10 to 76 +/- 10 mm Hg, and heart rate did not change (92 +/- 15 vs 92 +/- 14 bpm). At the end of a 48 to 72 hour titration to an optimal regimen, significant effects on CO (3.2 +/- 1.1 vs 4.5 +/- 1.3 L/min), PAD (24 +/- 12 vs 18 +/- 8 mm Hg), and MAP (84 +/- 10 vs 76 +/- 10 mm Hg) were still seen. The patients were restudied after 3 months of treatment. In contrast to reports of rapid development of tolerance to prazosin, we found continued beneficial effects on CO (3.0 +/- 1.3 vs 3.8 +/- 1.0 L/min) and PAD (23 +/- 12 vs 18 +/- 10 mm Hg), without significant change in MAP (81 +/- 11 vs 78 +/- 8 mm Hg). We found wide variability in the CO rise in response to prazosin, which was not accounted for by differences in plasma prazosin concentration. Systemic vascular resistance in the untreated state did correlate with the percentage change in CO. In addition, excessive lowering of the PAD appeared to blunt the CO response in some cases.
13例晚期充血性心力衰竭（CHF）患者接受了哌唑嗪治疗。首次给药后，心输出量（CO）（均值±标准差）从3.2±1.2升/分钟升至4.3±1.1升/分钟，肺动脉舒张压（PAD）从23±12毫米汞柱降至18±11毫米汞柱，平均动脉压（MAP）从85±10毫米汞柱降至76±10毫米汞柱，心率未改变（92±15次/分钟对92±14次/分钟）。在48至72小时滴定至最佳方案结束时，对CO（3.2±1.1对4.5±1.3升/分钟）、PAD（24±12对18±8毫米汞柱）和MAP（84±10对76±10毫米汞柱）仍有显著影响。治疗3个月后对患者进行复查。与关于对哌唑嗪快速产生耐受性的报道相反，我们发现对CO（3.0±1.3对3.8±1.0升/分钟）和PAD（23±12对18±10毫米汞柱）仍有持续有益作用，MAP无显著变化（81±11对78±8毫米汞柱）。我们发现对哌唑嗪反应时CO升高存在很大差异，这无法用血浆哌唑嗪浓度差异来解释。未治疗状态下的全身血管阻力确实与CO的变化百分比相关。此外，在某些情况下，PAD过度降低似乎会减弱CO反应。
