Smit A J, Meijer S, Wesseling H, Reitsma W D, Donker A J
Department of Medicine, University Hospital Groningen, The Netherlands.
Nephron. 1989;52(4):338-46. doi: 10.1159/000185674.
Renal hemodynamics and sodium excretion were determined before and during infusion of dopamine in doses ranging from 0.25 to 8 micrograms/kg/min in healthy volunteers (n = 15) and in patients with renal disease and moderately impaired renal function (n = 21, baseline glomerular filtration rate 34-85 ml/min). While in normal volunteers dopamine resulted in marked renal vasodilation (maximal fall in filtration fraction 24%), in patients with moderately impaired renal function, the renal vasodilatory response to dopamine was impaired (maximal fall in FF 13%) and was found to depend on baseline glomerular filtration rate. Infusion of dopamine in doses of 2 micrograms/kg/min and higher resulted in an increase in urinary sodium excretion, which was comparable for healthy volunteers and patients with renal disease. We conclude that dopamine results in a predominantly efferent glomerular vasodilation and, therefore, may be salutary in lowering intraglomerular hypertension. However, in patients with renal disease the renal hemodynamic response to dopamine infusion is impaired compared to healthy volunteers, while the natriuretic response is maintained.
在健康志愿者（n = 15）以及患有肾脏疾病且肾功能中度受损的患者（n = 21，基线肾小球滤过率为34 - 85 ml/分钟）中，于输注多巴胺前及输注过程中测定了肾血流动力学和钠排泄情况。多巴胺输注剂量范围为0.25至8微克/千克/分钟。在正常志愿者中，多巴胺可导致显著的肾血管舒张（滤过分数最大下降24%），而在肾功能中度受损的患者中，对多巴胺的肾血管舒张反应受损（滤过分数最大下降13%），且发现该反应取决于基线肾小球滤过率。以2微克/千克/分钟及更高剂量输注多巴胺会导致尿钠排泄增加，这在健康志愿者和肾病患者中相当。我们得出结论，多巴胺主要导致肾小球出球小动脉舒张，因此可能有助于降低肾小球内高压。然而，与健康志愿者相比，肾病患者对多巴胺输注的肾血流动力学反应受损，而利钠反应得以维持。
