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碳酸氢盐诱导的碱中毒对正常人体内尿素合成无影响。

No effect of bicarbonate-induced alkalosis on urea synthesis in normal man.

作者信息

Bjerrum K, Vilstrup H, Almdal T P, Ostergaard Kristensen L

机构信息

Division of Hepatology, Rigshospitalet, Copenhagen, Denmark.

出版信息

Scand J Clin Lab Invest. 1990 Apr;50(2):137-41. doi: 10.1080/00365519009089145.

Abstract

The effect of metabolic alkalosis was studied in 10 healthy volunteers. In each person urea synthesis was determined in two periods of 2 h as urinary excretion corrected for accumulation in body water and for intestinal hydrolysis. Infusion of bicarbonate (115 mmol/h) increased pH of the venous blood by 0.10 units. In four subjects fasting urea synthesis was 24 mmol N/h at normal pH and unaffected by alkalosis (mean difference +/- SED was 1.04 +/- 4.1). In six subjects alanine was infused so as to increase blood alanine concentration from 0.4 to 2.5 mmol/l and urea synthesis to 107 mmol N/h. Alkalosis did not change urea synthesis (mean difference +/- SED was 1.5 +/- 7.4 mmol N/h). The results favour the view that urea synthesis mainly serves to eliminate nitrogen, but do not support the hypothesis that urea synthesis is an important immediate and direct regulatory process in acute acid-base disturbances.

摘要

对10名健康志愿者的代谢性碱中毒效应进行了研究。对每个人在两个2小时时间段内测定尿素合成情况,以尿排泄量为基础,校正了体内水分蓄积和肠道水解的影响。输注碳酸氢盐(115 mmol/h)使静脉血pH值升高0.10个单位。在4名受试者中,正常pH值时空腹尿素合成量为24 mmol N/h,且不受碱中毒影响(平均差值±标准误为1.04±4.1)。在6名受试者中输注丙氨酸,使血丙氨酸浓度从0.4 mmol/l升至2.5 mmol/l,尿素合成量增至107 mmol N/h。碱中毒并未改变尿素合成(平均差值±标准误为1.5±7.4 mmol N/h)。结果支持尿素合成主要用于清除氮的观点,但不支持尿素合成是急性酸碱紊乱中重要的即时直接调节过程这一假说。

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