甘油致急性肾衰竭的肾血管收缩。大鼠离体灌注肾的研究。

K G Hofbauer, K Bauereiss, A Konrads, F Gross
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引用次数: 4

摘要

1. 肌内注射甘油(6.1 mol/l 10 ml/kg)可引起大鼠急性肾功能衰竭。2或4- 6小时后,分离右肾,用含有明胶制剂(Haemaccel, 35 g/l)的电解质溶液在90至100 mm Hg的单道系统中灌注1小时。2. 在急性肾功能衰竭大鼠的肾脏中,与未处理大鼠的对照肾脏相比,肾血管阻力在灌注开始后立即显著增加。在随后的30min灌注中,阻力逐渐下降,在灌注1 h时,阻力与对照肾脏相似或仅中度升高。3.尽管肾血管阻力降低,但灌注开始后肾小球滤过率仍明显高于未处理大鼠的对照肾脏。在随后的30min灌注中,阻力逐渐下降,在灌注1 h时,阻力与对照肾脏相似或仅中度升高。3.尽管肾血管阻力降低,但灌注1 h后肾小球滤过率仍明显受损,钠和水的部分重吸收以及对氨基马粪酸的分泌减少。急性肾功能衰竭大鼠肾脏的肾静脉肾素浓度和肾素释放量低于对照组。4. 这些结果表明,体内注射甘油后肾血管阻力的增加和肾素释放的刺激是肾外机制而不是肾内机制的结果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Renal vasoconstriction in glycerol-induced acute renal failure. Studies in the isolated perfused rat kidney.

1. Acute renal failure was produced in rats by the intramuscular injection of glycerol (6.1 mol/l 10 ml/kg). Either 2 or 4--6 h later the right kidney was isolated and perfused for 1 h with an electrolyte solution containing a gelatin preparation (Haemaccel, 35 g/l) at pressures between 90 and 100 mm Hg in a single-pass system. 2. In kidneys taken from rats with acute renal failure renal vascular resistance was markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly impaired after 1 h of perfusion and fractional reabsorption of sodium and water as well as the secretion of p-aminohippurate were diminished. Renal venous renin concentration and renin release were lower in kidneys taken from rats with acute renal failure than in the control experiments. 4. These results suggest that the increase in renal vascular resistance and the stimulation of renin release after injection of glycerol in vivo are the consequence of extra- rather than intra-renal mechanisms.

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