Differential effect of frusemide on renal medullary and cortical blood flow in the anaesthetised rat
Differential effect of frusemide on renal medullary and cortical blood flow in the anaesthetised rat
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DOI：
10.1111/j.1469-445x.2000.02064.x
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发表时间：
2000-11-01
影响因子：
2.7
通讯作者：
Sadowski, J
中科院分区：
文献类型：
--
作者：
Dobrowolski, L;Badzynska, B;Sadowski, J
除了已知的对肾小管运输的影响外，弗鲁塞米（呋塞米）已被证明可以影响肾循环。本研究在麻醉大鼠中检测了氟塞米（0.25或0.5 mg kg（-1）静脉注射，然后在1小时内输注相同剂量）对肾皮质和髓质循环的影响，激光多普勒血（细胞）通量测量。这些反应与同时测量的肾排泄和组织导纳的变化进行了比较，组织导纳是骨髓间质离子高张力的指标。肾血管对氟塞胺的反应显著，但不依赖于剂量。低剂量输注氟塞胺时，皮质通量降低11.5 +/- 0.9%，髓质通量降低32.3 +/- 3.5% （P < 0.001）。大剂量输注组分别下降13.5 +/- 1.4%和29.3 +/- 3.8% （P < 0.001）。低速和高速输注氟塞胺时，钠排泄量分别增加15倍（3.7 +/- 0.4 μ mol / min(-1)）和30倍（5.9 +/- 1.1 μ mol / min(-1)）。相比之下，髓质组织导纳的下降与两种剂量相似：最大分别下降13.4 +/- 1.4和10.9 +/- 0.9%。观察发现，在使用氟塞胺后，髓质内血流的急剧减少与该区域组织导纳的减少同时发生，而且髓质血液和导纳的变化都与剂量无关，这表明间质离子高渗性和血管阻力之间存在因果关系。我们认为，氟塞胺后髓组织NaCl的减少通过抑制局部血管扩张剂前列腺素的产生来抑制髓循环。
In addition to its known effect on renal tubular transport, frusemide (furosemide) has been shown to affect renal circulation. This study in the anaesthetised rat examined the influence of frusemide (bolus 0.25 or 0.5 mg kg(-1) I.V., then infusion delivering the same dose over 1 h) on renal cortical and medullary circulation measured as laser-Doppler blood (cell) flux. The responses were compared with simultaneously measured changes in renal excretion and in the tissue admittance, an index of medullary ionic hypertonicity of the interstitium. Renal vascular responses to frusemide were significant but not dose dependent. During low-dose frusemide infusion cortical flux decreased 11.5 +/- 0.9% and medullary flux decreased 32.3 +/- 3.5% (difference significant at P < 0.001). During high-dose infusion the decreases were by 13.5 +/- 1.4 and 29.3 +/- 3.8%, respectively (difference significant at P < 0.001). Sodium excretion increased 15-fold (by 3.7 +/- 0.4 mu mol min(-1)) and 30-fold (by 5.9 +/- 1.1 mu mol min(-1)) during low- and high-rate infusion of frusemide, respectively. By contrast, medullary tissue admittance decreased similarly with the two doses: maximally by 13.4 +/- 1.4 and 10.9 +/- 0.9%, respectively. The observations that an exaggerated post-frusemide decrease in blood flow within the medulla coincided with decreasing tissue admittance in this zone and that neither medullary blood now nor admittance changes were related to the dose suggest a causal relationship between interstitial ionic hypertonicity and vascular resistance. We propose that the post-frusemide decrease in medullary tissue NaCl depressed medullary circulation by inhibiting local generation of vasodilator prostaglandins.