Pesquero J, Alfaro V, Palacios L
Departamento de Fisiología, Facultad de Biología, Universidad de Barcelona, Spain.
Can J Physiol Pharmacol. 2000 Oct;78(10):774-80.
The present study evaluated the acid-base status of anemic rats by using two approaches of acid-base analysis: one based on the base excess (BE) calculation and the other based on Stewart's physicochemical analysis. Two sets of experimental data, derived from two different methods of inducing anemia, were used: repetitive doses of phenylhydrazine (PHZ) and bleeding (BL). A significant uncompensated respiratory alkalosis was found in both groups of anemic rats. BE increased slightly, whereas strong ion difference ([SID]) and weak acid buffers ([A(TOT)]) remained unchanged in anemic rats. The reasons for the absence of compensation for hypocapnia and the differences in the behaviour of acid-base variables are discussed. BE increase was considered paradoxical; its calculation was affected by the experimental conditions and BE had little physiological relevance during anemia. The absence of metabolic renal compensation in anemic rats could be due to a lower pH in the kidney due to anemic hypoxia. Finally, the changes in buffer strength related to low Hb and low P(CO2) might influence plasma [SID] through counteracted shifts of strong ions between erythrocytes and plasma, finally resulting in unchanged [SID] during anemia.
一种基于碱剩余（BE）计算，另一种基于斯图尔特物理化学分析。使用了两组来自两种不同贫血诱导方法的实验数据：重复剂量的苯肼（PHZ）和放血（BL）。在两组贫血大鼠中均发现显著的未代偿性呼吸性碱中毒。贫血大鼠的BE略有增加，而强离子差（[SID]）和弱酸缓冲剂（[A(TOT)]）保持不变。讨论了低碳酸血症未得到代偿的原因以及酸碱变量行为的差异。BE增加被认为是矛盾的；其计算受实验条件影响，且在贫血期间BE几乎没有生理相关性。贫血大鼠缺乏代谢性肾代偿可能是由于贫血性缺氧导致肾脏pH值降低。最后，与低血红蛋白和低P(CO2)相关的缓冲强度变化可能通过红细胞和血浆之间强离子的抵消性转移影响血浆[SID]，最终导致贫血期间[SID]保持不变。
