Serizawa T, Hirata Y, Kohmoto O, Iizuka M, Matsuoka H, Sato H, Takahashi T, Mochizuki T, Ishii M, Sugimoto T
Second Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
Jpn Heart J. 1988 Mar;29(2):143-9. doi: 10.1536/ihj.29.143.
Acute hemodynamic and humoral effects of synthesized alpha human atrial natriuretic polypeptide (alpha-hANP, 0.025 microgram/kg/min for 40 min) on 6 patients with severe congestive heart failure were assessed. Plasma alpha-hANP concentration was high in patients and increased further (from 463 +/- 360 to 1,282 +/- 670 pg/ml, mean +/- SD, p less than 0.01) following alpha-hANP infusion, but plasma norepinephrine (1,030 +/- 865 to 971 +/- 785 pg/ml) was not changed. Increases in urine output (1.0 +/- 0.8 to 2.6 +/- 2.3 ml/min) and Na+ excretion rate (87 +/- 89 to 257 +/- 211 mEq/min/m2) were statistically insignificant. A significant reduction was induced in mean aortic pressure (99 +/- 25 to 96 +/- 26 mmHg, p less than 0.05), mean right atrial pressure (11 +/- 9 to 7 +/- 8 mmHg, p less than 0.01), mean pulmonary arterial pressure (39 +/- 13 to 33 +/- 12 mmHg, p less than 0.05) and mean pulmonary capillary wedge pressure (27 +/- 8 to 20 +/- 7 mmHg, p less than 0.01). Heart rate, cardiac index, systemic vascular resistance and pulmonary vascular resistance were not altered. In conclusion, alpha-hANP induced decreases in left ventricular filling pressure and rightside heart pressure which were attributed to venodilatation rather than natriuresis in patients with congestive heart failure. Preserved cardiac output with decreased preload suggested that alpha-hANP improved cardiac function.
评估了合成的α-人心房利钠多肽(α-hANP,以0.025微克/千克/分钟的剂量持续输注40分钟)对6例重度充血性心力衰竭患者的急性血流动力学和体液影响。患者血浆α-hANP浓度较高,α-hANP输注后进一步升高(从463±360皮克/毫升升至1282±670皮克/毫升,均值±标准差,p<0.01),但血浆去甲肾上腺素浓度(从1030±865皮克/毫升降至971±785皮克/毫升)未发生变化。尿量(从1.0±0.8毫升/分钟增至2.6±2.3毫升/分钟)和钠排泄率(从87±89毫当量/分钟/平方米增至257±211毫当量/分钟/平方米)的增加无统计学意义。平均主动脉压(从99±25毫米汞柱降至96±26毫米汞柱,p<0.05)、平均右心房压(从11±9毫米汞柱降至7±8毫米汞柱,p<0.01)、平均肺动脉压(从39±13毫米汞柱降至33±12毫米汞柱,p<0.05)和平均肺毛细血管楔压(从27±8毫米汞柱降至20±7毫米汞柱,p<0.01)均显著降低。心率、心脏指数、全身血管阻力和肺血管阻力未改变。总之,α-hANP可使充血性心力衰竭患者左心室充盈压和右侧心脏压力降低,这归因于静脉扩张而非利钠作用。前负荷降低但心输出量保持不变,提示α-hANP改善了心脏功能。