Kveim M, Nesbakken R
Scand J Clin Lab Invest. 1979 Nov;39(7):653-8. doi: 10.1080/00365517909108870.
Plasma acetate and lactate, as well as acid-base-parameters were followed during acetate (dogs I-V) or lactate (dogs VI-X) loading during stable hypotension (mean arterial blood pressure 30 mmHg). Acetate or lactate were infused at a constant rate of 4 mmol/kg/h as 0.5 mol/l solutions (50% as the sodium salt, 50% as the free acid) without simultaneous treatment of the volume deficit. The acetate metabolizing capacity was well preserved even in profound haemorrhagic shock. The actual loads were rapidly removed, while the equivalent lactate loads caused progressive accumulation of the lactate ion. Acetate loading did not aggravate the lactic acidosis, and the acid-base-parameters showed a more favourable development during acetate loading than during lactate loading. Acetate may thus be given during haemorrhagic shock without the same risk of accumulation that is carried by the equivalent amounts of lactate.
在稳定的低血压状态（平均动脉血压30 mmHg）下，对醋酸盐（I-V组犬）或乳酸盐（VI-X组犬）负荷期间的血浆醋酸盐和乳酸盐以及酸碱参数进行了监测。醋酸盐或乳酸盐以4 mmol/kg/h的恒定速率作为0.5 mol/l溶液输注（50%为钠盐，50%为游离酸），且未同时处理容量不足问题。即使在严重失血性休克中，醋酸盐的代谢能力也得到了很好的保留。实际负荷被迅速清除，而等量的乳酸盐负荷则导致乳酸离子的进行性积累。醋酸盐负荷并未加重乳酸性酸中毒，且酸碱参数在醋酸盐负荷期间比乳酸盐负荷期间显示出更有利的变化。因此，在失血性休克期间给予醋酸盐时，不会有等量乳酸盐所带来的相同的蓄积风险。
