Assessment of intrarenal blood flow distribution and sodium excretion using contrast ultrasonography

肾内血流的分布在各种肾功能调节中的重要性，如尿浓度和钠排泄，已被充分认识。然而，还没有可靠的方法来测量体内肾脏中的局部血流量。我们研究了局部肾血流量和体内钠排泄之间的相关性，采用超声造影结合主动脉内注射超声处理的5%白蛋白在杂种狗。5%白蛋白0.15-0.25ml/kg可获得满意的肾实质超声强化。此外，内/外肾皮质的峰值强度比显着增加，在肾内注入乙酰胆碱。静脉注射一氧化氮（NO）合成抑制剂L-硝基精氨酸甲酯（L-NAME）可显著抑制等渗盐水扩张急性细胞外容积引起的利钠反应，但不改变肾血浆总流量和肾皮质血流分布。用血管紧张素Ⅱ受体（AT_1）拮抗剂L-158，809预处理可完全消除L-NAME的这种抑制作用，提示在NO合成抑制过程中，肾对急性细胞外容积扩张的排泄反应降低是血管紧张素Ⅱ依赖性的。静脉注射半乳糖/棕榈酸在肾血管或实质疾病患者中的应用。因此，这些结果表明，区域肾血流量和钠排泄之间的相关性，可以检测在人类的信号增强的定量分析。

The importance of the distribution of intrarenal blood flow in the regulation of various renal functions, such as urine concentration and sodium excretion, has been well recognized. However, there have been no reliable methods to measure local blood flow in the kidney in vivo. We studied the correlations between regional renal Blood flow and sodium excretion in vivo using contrast ultrasonograpy combined with intraaortic injection of a sonicated 5% albumin in mongrel dogs. Satisfactory sonographic enhancement in renal parenchyma was obtained by the sonicated 5% albumin of 0.15-0.25ml/kg. Furthermore, the inner/outer renal cortex ratio of peak intensity significantly increased during the intrarenal acetylcholine infusion. Intravenous infusion of nitric oxide (NO) synthesis inhibitor, N^G-nitro-L-arginine methyl ester (L-NAME), at a low dose significantly inhibited the natriuretic response to acte extracellular volume expansion with isotonic saline without altering total renal plasma flow and the distribution of renal cortical blood flow. This inhibitory effect of L-NAME was completely abolished by the pretreatment with angiotensin II receptor (AT_1) antagonist, L-158,809, suggesting an angiotensin II dependency of the reduced renal excretory response to acute extracellular volume expansion during NO synthesis inhibition.In addition, we obtained effective signal enhancement in color Doppler flow imaging in the kidney with an intravenous injection of the contrast agent consisting of galactose/palmitic acid in patients with renal vascular or parenchymal diseases. Thus, these results suggest that the correlations between regional renal blood flow and sodium excretion can be detected by a quantitative analysis of signal enhancement in humans.