[使用放射造影剂后肾脏多巴胺分泌增加]。

J Santos, V Araújo, L Moura, P Serrão, L Guerra, J Maciel, M Pestana
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引用次数: 0

摘要

由造影造影剂(CA)引起的肾血管收缩和抗尿钠可能通过外源性多巴胺的施用而拮抗。然而,CA对肾脏多巴胺合成活性的影响尚未见研究。这项研究评估了每日尿中多巴胺的排泄量,多巴胺是其前体。l - 3,4 -二羟基苯胺(L-DOPA)及其代谢物(酸3,4 -二羟基苯基乙酸,DOPAC;高香草酸,HVA)在给药前24小时和给药后48小时的非离子和低摩尔(洛丙胺)CA患者(n = 10;平均年龄61.3±4.3岁)行冠状动脉造影。尿中去甲肾上腺素(交感神经活动的标志)的排泄也在同一时期进行了评估。给药后肌酐(Ccr)和尿钠(UNa+)排泄量下降(Ccr为79.2 +/- 10.2 vs 72.2 +/- 9.6 ml/min/1.73 m2, p < 0.05;UNa + 112.8 + / - 9.6 vs 61.7 + / - 25.1更易与24 h, p < 0.05)。相反,在给药后24 h内尿钾排泄量增加(31.7 +/- 5.2 vs 103.8 +/- 10.8 mmol/24 h, p < 0.05)。在给予CA后的24小时内,尿中多巴胺和去甲肾上腺素的排泄量增加(多巴胺,1260.2 +/- 196.8 vs 1571.5 +/- 170.2 mmol/24 h p < 0.5;去甲肾上腺素186 +/- 36.6 mmol/24 h, p < 0.05)。相反,给药后尿L-DOPA排泄量降低(115.4 +/- 25.5 vs 80.5 +/- 13.2 mmol/24 h, p < 0.05)。这些结果表明,在给予CA后,尿中多巴胺/左旋多巴比值增加(12.2 +/- 1.5 vs 22.2 +/- 4.5 mmol/24 h, p < 0.05)。总之,CA的施用伴随着肾脏多巴胺分泌的增加,在这些情况下,多巴胺可能作为代偿性利钠激素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[An increase in renal dopamine production after the administration of radiographic contrast agents].

Renal vasoconstriction and anti-natriuresis conditioned by radiographic contrast agents (CA) may be antagonised by the administration of exogenous dopamine. However, the influence of CA on the activity of renal synthesis of dopamine has not been studied. This study assessed the daily urinary excretion of dopamine, its precursor. L-3, 4-dihydroxyphenylaline (L-DOPA), and its metabolites (acid 3, 4-dihydroxyphenylacetic, DOPAC; homovanillic acid, HVA) 24 hours before and 48 hours following administration of a non ionic and hyposmolar (lopromide) CA in patients (n = 10; average age 61.3 +/- 4.3 years) submitted to coronary angiography. Urinary excretion of noradrenalin, a marker of sympathetic activity, was also assessed during the same period. The deputation of creatinine (Ccr) and the urinary excretion of sodium (UNa+) lowered after the administration of the CA (Ccr, 79.2 +/- 10.2 vs 72.2 +/- 9.6 ml/min/1.73 m2, p < 0.05; UNa+, 112.8 +/- 9.6 vs 61.7 +/- 25.1 mmol/24 h, p < 0.05). On the contrary, the urinary excretion of potassium increased in the period of 24 h following the administration of the AC (31.7 +/- 5.2 vs 103.8 +/- 10.8 mmol/24 h, p < 0.05). There was an increase in the urinary excretion of dopamine as well as noradrelalin during the 24 hour period following the administration of the CA (dopamine, 1260.2 +/- 196.8 vs 1571.5 +/- 170.2 mmol/24 h p < 0.5; noradrenalin, 186 +/- 36.6 mmol/24 h, p < 0.05). On the contrary, the urinary excretion of L-DOPA lowered after the administration of the CA (115.4 +/- 25.5 vs 80.5 +/- 13.2 mmol/24 h, p < 0.05). These results conditioned an increase in the dopamine/L-DOPA ratio in the urine, after the administration of the CA (12.2 +/- 1.5 vs 22.2 +/- 4.5 mmol/24 h, p < 0.05). In conclusion, the administration of CA is accompanied by an increase in the renal production of dopamine which, in these conditions, may act as a compensatory natriuretic hormone.

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