Richer M, Robert S, Lebel M
Ecole de pharmacie, Université Laval, Pfizer, Canada.
Crit Care Med. 1996 Jul;24(7):1150-6. doi: 10.1097/00003246-199607000-00014.
To characterize the effects of pressor doses of norepinephrine and low-dose dopamine (3 micrograms/kg/min) on renal hemodynamics in man, as well as to determine the clinical relevance of combining dopamine with norepinephrine.
Prospective, single-blind, randomized study.
Clinical research unit of a tertiary care hospital. SUBJECTS. Six healthy male volunteers ranging in age between 20 and 28 yrs.
The subjects were assigned randomly to four treatments (1 wk apart) in which renal hemodynamics and electrolyte excretion were assessed. Treatments consisted of 180-min infusions of the following: a) 0.9% sodium chloride (control); b) pressor doses of norepinephrine; c) dopamine at 3 micrograms/kg/min; and d) pressor doses of norepinephrine and dopamine at 3 micrograms/kg/min. Pressor doses of norepinephrine was defined as doses required to increase mean arterial pressure (MAP) by 20 mm Hg.
Glomerular filtration rate and renal blood flow were derived from inulin and para-aminohippurate clearances, respectively. Urine output and urine solute excretion were also determined. The mean norepinephrine dose required to increase MAP by 22 +/- 2 mm Hg was 118 +/- 30 ng/kg/min (range 76 to 164). After the addition of dopamine, similar doses of norepinephrine resulted in an MAP increase of 15 +/- 4 mm Hg. Glomerular filtration rate and urine output were comparable under all conditions. The infusion of norepinephrine decreased renal blood flow from 1241 +/- 208 to 922 +/- 143 mL/min/1.73 m2 (p = .03). The addition of dopamine returned renal blood flow to baseline values. The clearance of urine sodium increased significantly with the infusion of dopamine alone (p = .03). All subjects completed the four treatment periods. Adverse events, manifested mostly as palpitations and flushing, were rare and self-limiting.
The addition of dopamine (3 micrograms/kg/min) to pressor doses of norepinephrine normalized renal blood flow in healthy volunteers. These hemodynamic changes were not reflected in urine output and glomerular filtration rate; hence, these monitoring parameters may be unreliable indicators of renal function in the setting of vasopressor therapy. In addition, systemic effects were observed with dopamine (3 micrograms/kg/min), as indicated by a decrease in MAP.
描述去甲肾上腺素升压剂量和低剂量多巴胺（3微克/千克/分钟）对人体肾血流动力学的影响，并确定多巴胺与去甲肾上腺素联合应用的临床相关性。
前瞻性、单盲、随机研究。
三级护理医院的临床研究单位。
6名年龄在20至28岁之间的健康男性志愿者。
受试者被随机分配接受四种治疗（间隔1周），评估肾血流动力学和电解质排泄情况。治疗包括180分钟输注以下物质：a）0.9%氯化钠（对照）；b）去甲肾上腺素升压剂量；c）3微克/千克/分钟的多巴胺；d）去甲肾上腺素升压剂量和3微克/千克/分钟的多巴胺。去甲肾上腺素的升压剂量定义为使平均动脉压（MAP）升高20毫米汞柱所需的剂量。
肾小球滤过率和肾血流量分别通过菊粉和对氨基马尿酸清除率得出。还测定了尿量和尿溶质排泄量。使MAP升高22±2毫米汞柱所需的平均去甲肾上腺素剂量为118±30纳克/千克/分钟（范围76至164）。加入多巴胺后，相似剂量的去甲肾上腺素使MAP升高15±4毫米汞柱。在所有情况下，肾小球滤过率和尿量相当。输注去甲肾上腺素使肾血流量从1241±208降至922±143毫升/分钟/1.73平方米（p = 0.03）。加入多巴胺后肾血流量恢复至基线值。单独输注多巴胺时尿钠清除率显著增加（p = 0.03）。所有受试者均完成了四个治疗期。不良事件主要表现为心悸和潮红，很少见且为自限性。
在去甲肾上腺素升压剂量基础上加用多巴胺（3微克/千克/分钟）可使健康志愿者的肾血流量恢复正常。这些血流动力学变化未反映在尿量和肾小球滤过率上；因此，在血管升压药治疗时，这些监测参数可能是肾功能的不可靠指标。此外，如MAP降低所示，观察到多巴胺（3微克/千克/分钟）有全身效应。
