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给予氨基甲酸盐是否会急性导致非碳酸氢盐缓冲剂的回滴定?

Does the administration of carbicarb lead acutely to back-titration of non-bicarbonate buffers?

作者信息

Kamel K S

机构信息

Division of Nephrology, St. Michael's Hospital, Toronto, Canada.

出版信息

Clin Nephrol. 1996 Aug;46(2):112-6.

PMID:8869788
Abstract

OBJECTIVE

We have recently demonstrated in a model of acute metabolic acidosis in rats that the administration of NaHCO3 does not lead acutely to back-titration of non-bicarbonate buffers. Carbicarb is a new alkalinizing agent that has been proposed as a replacement for NaHCO3 in the treatment of metabolic acidosis. Hence, the purpose of this study was to examine the impact of carbicarb on back-titration of non-bicarbonate buffers.

METHODS

Rats were anaesthetized, intubated and ventilated to a PCO2 of approximately 30 mmHg. Acute metabolic acidosis was induced by the infusion over 1 hour of 3.5 mmol of hydrochloric acid. After a 20 min equilibration period, 3 groups of rats (n = 7 in each group) were examined. Rats in groups I received 0.75 meq of Na from 1 M carbicarb solution as an intravenous bolus, rats in group II received equimolar NaCl, while rats in group III were used as time controls. Calculations were performed to quantitate the amount of HCO3- that was retained in the ECF volume and the amount that was titrated with H+ and excreted as "acid-base" CO2. "Acid-base" CO2 was considered as the amount of CO2 that was excreted in excess of what would be produced during metabolism.

RESULTS

As compared to the NaCl and the time control groups, the administration of carbicarb led to significant alkalinization of the ECF, pH rose from 7.23 +/- 0.02 to 7.34 +/- 0.03. Of the 0.75 mmol of carbicarb that was administered, 0.61 +/- 0.05 mmol (70%) was retained in ECF. There was virtually no "acid-base" CO2 produced.

CONCLUSIONS

The administration of carbicarb does not lead acutely to back-titration of non-bicarbonate buffers especially under conditions of fixed ventilation.

摘要

目的

我们最近在大鼠急性代谢性酸中毒模型中证明,给予碳酸氢钠不会急性导致非碳酸氢盐缓冲液的反向滴定。卡比卡(Carbicarb)是一种新的碱化剂,已被提议作为治疗代谢性酸中毒时替代碳酸氢钠的药物。因此,本研究的目的是检查卡比卡对非碳酸氢盐缓冲液反向滴定的影响。

方法

将大鼠麻醉、插管并通气,使动脉血二氧化碳分压维持在约30 mmHg。通过在1小时内输注3.5 mmol盐酸诱导急性代谢性酸中毒。在20分钟平衡期后,检查3组大鼠(每组n = 7)。I组大鼠静脉推注1 M卡比卡溶液中的0.75 meq钠,II组大鼠接受等摩尔的氯化钠,而III组大鼠用作时间对照。进行计算以定量细胞外液(ECF)中保留的碳酸氢根离子量以及与氢离子滴定并作为“酸碱”二氧化碳排出的量。“酸碱”二氧化碳被视为排出的二氧化碳量超过代谢过程中产生的量。

结果

与氯化钠组和时间对照组相比,给予卡比卡导致细胞外液显著碱化,pH从7.23±0.02升至7.34±0.03。给予的0.75 mmol卡比卡中,0.61±0.05 mmol(70%)保留在细胞外液中。几乎没有产生“酸碱”二氧化碳。

结论

给予卡比卡不会急性导致非碳酸氢盐缓冲液的反向滴定,特别是在固定通气条件下。

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