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碳酸氢钠预负荷对缺血性肾衰竭的影响。

Effect of sodium bicarbonate preloading on ischemic renal failure.

作者信息

Atkins J L

出版信息

Nephron. 1986;44(1):70-4. doi: 10.1159/000183915.

Abstract

Rats pretreated with sodium bicarbonate were functionally protected from the damage of bilateral renal artery occlusion. The rise in serum creatinine (day 1 minus day 0) during the first 24 h after ischemia was 2.88 +/- 0.28 mg% in the bicarbonate-loaded animals versus 3.90 +/- 0.26 mg% in their matched controls (p less than or equal to 0.01). Pretreatment with acetazolamide produced a similar alkaline urine as the bicarbonate loading (pH 8.3 vs. 7.0 in controls) and a similar degree of protection (delta creatinine 2.85 +/- 0.41 vs. 4.23 +/- 0.26 mg%; p less than or equal to 0.01). A direct effect of sodium loading was excluded by comparing NH4HCO3 with NaHCO3 loading and observing no difference in delta creatinine levels after ischemia (3.39 +/- 0.69 vs. 3.20 +/- 0.61 mg%). These data indicate that NaHCO3 protects in this model of acute renal failure and further suggest that the mechanism of protection is not related to either systemic alkalosis or sodium loading.

摘要

用碳酸氢钠预处理的大鼠在功能上受到保护,免受双侧肾动脉闭塞的损伤。缺血后最初24小时内,碳酸氢钠负荷组动物血清肌酐的升高(第1天减去第0天)为2.88±0.28mg%,而匹配对照组为3.90±0.26mg%(p≤0.01)。用乙酰唑胺预处理产生的碱性尿液与碳酸氢钠负荷相似(pH值分别为8.3和7.0),保护程度也相似(肌酐变化量分别为2.85±0.41和4.23±0.26mg%;p≤0.01)。通过比较碳酸氢铵和碳酸氢钠负荷,并观察缺血后肌酐变化量水平无差异(分别为3.39±0.69和3.20±0.61mg%),排除了钠负荷的直接影响。这些数据表明,碳酸氢钠在该急性肾衰竭模型中具有保护作用,并进一步表明保护机制与全身碱中毒或钠负荷均无关。

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