Gotshall R W
Am J Physiol. 1983 Dec;245(6):F687-90. doi: 10.1152/ajprenal.1983.245.6.F687.
The effect of intrarenal arterial infusion of hyperoncotic dextran on renal hemodynamics and excretion was studied in anesthetized dogs. To examine the role of glomerular filtration and tubular flow in the hemodynamic response, several kidney models were employed. Nonfiltering kidneys (NFK) were produced by combined ischemia and ureteral obstruction (UO). Additionally, kidneys with only UO and a lack of filtration as well as kidneys with only ischemia and glomerular filtration were studied. Renal blood flow in normal kidneys was increased by hyperoncotic dextran from 357 +/- 47 to 486 +/- 65 ml X min-1 X 100 g-1, with a corresponding decrease in renal vascular resistance. Ischemic kidneys responded likewise to the dextran infusion, increasing renal blood flow from 261 +/- 31 to 339 +/- 29 ml X min-1 X 100 g-1. Glomerular filtration rate was reduced by the dextran infusion from 80.1 +/- 7.9 to 60.7 +/- 6.6 in normal kidneys and from 31.8 +/- 9.6 to 20.2 +/- 5.8 ml X min-1 X 100 g-1 in ischemic kidneys. Urine flow and sodium excretion were also reduced in these kidneys. In contrast, both NFK and UO, which lacked filtration and tubular flow, did not vasodilate in response to dextran. Renal blood flow remained unchanged from control values (NFK: 146 +/- 6, UO: 111 +/- 22 ml X min-1 X 100 g-1) in these kidneys. These experiments show that the renal vascular response to hyperoncotic dextran is not due to a change in blood volume or viscosity nor to a direct pharmacologic action of dextran. The most likely explanation is that hyperoncotic dextran alters tubuloglomerular feedback control of renal vascular resistance by decreasing filtration and altering tubular flow and/or composition. However, the involvement of another intrarenal vasodilatory system cannot be discounted.
在麻醉犬身上研究了肾内动脉输注高渗右旋糖酐对肾脏血流动力学和排泄的影响。为了研究肾小球滤过和肾小管流量在血流动力学反应中的作用，采用了几种肾脏模型。通过联合缺血和输尿管梗阻（UO）制作无滤过功能的肾脏（NFK）。此外，还研究了仅存在输尿管梗阻且无滤过功能的肾脏以及仅存在缺血和肾小球滤过功能的肾脏。正常肾脏的肾血流量因高渗右旋糖酐而从357±47增加至486±65 ml·min⁻¹·100 g⁻¹，肾血管阻力相应降低。缺血性肾脏对右旋糖酐输注的反应类似，肾血流量从261±31增加至339±29 ml·min⁻¹·100 g⁻¹。正常肾脏中，右旋糖酐输注使肾小球滤过率从80.1±7.9降至60.7±6.6，缺血性肾脏中则从31.8±9.6降至20.2±5.8 ml·min⁻¹·100 g⁻¹。这些肾脏的尿流量和钠排泄也减少。相比之下，缺乏滤过和肾小管流量的NFK和UO对右旋糖酐无血管舒张反应。这些肾脏的肾血流量与对照值相比保持不变（NFK：146±6，UO：111±22 ml·min⁻¹·100 g⁻¹）。这些实验表明，肾脏对高渗右旋糖酐的血管反应并非由于血容量或粘度的改变，也不是由于右旋糖酐的直接药理作用。最可能的解释是，高渗右旋糖酐通过减少滤过、改变肾小管流量和/或成分来改变肾血管阻力的球管反馈控制。然而，不能排除另一种肾内血管舒张系统的参与。
