Hoogenberg K, Smit A J, Girbes A R
Department of Internal Medicine, University Hospital Groningen, The Netherlands.
Crit Care Med. 1998 Feb;26(2):260-5. doi: 10.1097/00003246-199802000-00022.
To assess the effects of low-dose dopamine on norepinephrine-induced renal and systemic vasoconstriction in normotensive healthy subjects.
On separate days, either a low-dose dopamine (4 microg/kg/min) or a placebo (5% glucose) infusion was added in a single, blinded, randomized order to incremental norepinephrine infusions of 40, 80, and 150 ng/kg/min over a 60-min period each.
Outpatient clinic of a university-affiliated hospital.
Normotensive healthy volunteers.
Infusions of norepinephrine and dopamine.
Blood pressure and heart rate were measured with a semiautomated device, and glomerular filtration rate and effective renal plasma flow were determined with constant infusions of 125I-iothalamate and 131I-hippurate, respectively. Norepinephrine alone progressively increased mean arterial pressure to pressor levels, whereas this effect was attenuated by the addition of dopamine (p < .05 vs. norepinephrine alone). Glomerular filtration rate increased during lower norepinephrine doses and did not decrease at the highest norepinephrine dose. Addition of dopamine further increased glomerular filtration rate. Effective renal plasma flow decreased with each norepinephrine alone infusion step, but this decrease was completely prevented by concomitant dopamine infusion (p < .01 vs. norepinephrine). Sodium excretion tended to decrease with norepinephrine, but increased two- to three-fold after addition of dopamine (p < .01 vs. norepinephrine alone).
In healthy man, norepinephrine causes a large decrease in renal plasma flow but not in glomerular filtration rate. Concomitant dopamine administration prevents this decrease in renal plasma flow, increases sodium excretion, and also attenuates the norepinephrine-induced systemic blood pressure increase. These findings warrant further clinical evaluation of the effect of concomitant low-dose dopamine and norepinephrine administration in critically ill patients.
评估小剂量多巴胺对血压正常的健康受试者中去甲肾上腺素诱导的肾血管和全身血管收缩的影响。
在不同日期,以单次、盲法、随机顺序,在60分钟内分别将小剂量多巴胺(4微克/千克/分钟)或安慰剂(5%葡萄糖)输注添加到递增的去甲肾上腺素输注中,去甲肾上腺素输注速率分别为40、80和150纳克/千克/分钟。
大学附属医院门诊。
血压正常的健康志愿者。
去甲肾上腺素和多巴胺输注。
使用半自动设备测量血压和心率,分别通过持续输注125I-碘肽酸盐和131I-马尿酸盐来测定肾小球滤过率和有效肾血浆流量。单独使用去甲肾上腺素可使平均动脉压逐渐升高至升压水平,而添加多巴胺可减弱这种作用(与单独使用去甲肾上腺素相比,p < 0.05)。在较低剂量去甲肾上腺素时肾小球滤过率增加,在最高剂量去甲肾上腺素时未降低。添加多巴胺进一步增加了肾小球滤过率。单独每次输注去甲肾上腺素时有效肾血浆流量均降低,但同时输注多巴胺可完全防止这种降低(与单独使用去甲肾上腺素相比,p < 0.01)。去甲肾上腺素使钠排泄倾向于减少,但添加多巴胺后增加了两到三倍(与单独使用去甲肾上腺素相比,p < 0.01)。
在健康男性中,去甲肾上腺素可导致肾血浆流量大幅降低,但不会使肾小球滤过率降低。同时给予多巴胺可防止肾血浆流量降低,增加钠排泄,并减弱去甲肾上腺素引起的全身血压升高。这些发现值得对危重症患者同时给予小剂量多巴胺和去甲肾上腺素的效果进行进一步临床评估。