Pavoni V, Verri M, Ferraro L, Volta C A, Paparella L, Capuzzo M, Pavanelli L, Buccoliero C, Beani L, Alvisi R, Gritti G
Dipartimento di Scienze Biomediche e Terapie Avanzate, Universitá degli Studi di Ferrara, Azienda Ospedaliera S. Anna, Italy.
Kidney Int Suppl. 1998 May;66:S75-80.
To evaluate plasma dopamine concentration and the effects of low doses infusion on urinary output after abdominal vascular surgery in patients with renal function impairment we performed a prospective clinical study. Twenty hemodynamically stable patients (mean age 66.6 years), with serum creatinine concentration < 2 mg %, who undergoing general anesthesia for major vascular surgery participated. A low dose of dopamine (3 micrograms/kg/min) was administrated to patients with postoperative protracted urinary output < 0.5 ml/kg/hr for at least eight hours. Plasmatic determinations were taken at T0 (no dopamine administration), when urinary output began to increase, or if not, after two hours (T1), at eight (T2), and 24 (T3) hours after the beginning of infusion. After 24 hours the dopamine infusion was stopped and the patient's plasmatic level was measured four hours later (T4). Dopamine plasma concentrations were measured using high-performance liquid chromatography. Plasma dopamine concentration increased in all patients and reached a steady state at T2 (T2 = 76.41 +/- 16.84 ng/ml). Dopamine induced a concentration-dependent increase in urinary output (T0 = 0.45 +/- 0.14; T1 = 1.49 +/- 1.11; T2 = 2.34 +/- 1.44; T3 = 1.57 +/- 0.57; T4 = 0.85 +/- 0.7 ml/kg/hr). Three patients did not have an enhanced urinary output after dopamine infusion; they did have a prolonged clamping time and operation time (162 +/- 24 and 570 +/ 30 min, respectively). We conclude that low dose dopamine induces a dose-dependent increase of urinary output. This phenomenon also has been found in patients when their plasma concentration had not yet reached the steady-state. Lack of responsiveness to dopamine suggests a renal function impairment probably due to the prolonged aortic clamping time.
为评估肾功能损害患者腹部血管手术后的血浆多巴胺浓度以及小剂量多巴胺输注对尿量的影响,我们进行了一项前瞻性临床研究。20例血流动力学稳定的患者(平均年龄66.6岁)参与其中,这些患者血清肌酐浓度<2mg%,因重大血管手术接受全身麻醉。对于术后持续尿量<0.5ml/kg/hr至少8小时的患者,给予小剂量多巴胺(3微克/千克/分钟)。在T0(未给予多巴胺)、尿量开始增加时(若未增加,则在输注开始后2小时)(T1)、8小时(T2)和24小时(T3)采集血样测定。24小时后停止多巴胺输注,4小时后测量患者的血浆水平(T4)。使用高效液相色谱法测量多巴胺血浆浓度。所有患者的血浆多巴胺浓度均升高,并在T2达到稳态(T2 = 76.41±16.84纳克/毫升)。多巴胺使尿量呈浓度依赖性增加(T0 = 0.45±0.14;T1 = 1.49±1.11;T2 = 2.34±1.44;T3 = 1.57±0.57;T4 = 0.85±0.7毫升/千克/小时)。3例患者在多巴胺输注后尿量未增加;他们的夹闭时间和手术时间延长(分别为162±24分钟和570±30分钟)。我们得出结论,小剂量多巴胺可使尿量呈剂量依赖性增加。在患者血浆浓度尚未达到稳态时也发现了这种现象。对多巴胺无反应提示可能由于主动脉夹闭时间延长导致肾功能损害。