Krbec Martin, Waldauf Petr, Zadek Francesco, Brusatori Serena, Zanella Alberto, Duška František, Langer Thomas
Department of Anaesthesia and Intensive Care Medicine, The Third Faculty of Medicine, Charles University and FNKV University Hospital, Prague, Czechia.
Department of Pathophysiology and Transplantation, University of Milan, Milan, Italy.
Front Physiol. 2022 Oct 21;13:1009378. doi: 10.3389/fphys.2022.1009378. eCollection 2022.
Non-carbonic buffer power (β) of blood is a pivotal concept in acid-base physiology as it is employed in several acid-base evaluation techniques, including the Davenport nomogram and the Van Slyke equation used for Base excess estimation in blood. So far, β has been assumed to be independent of metabolic acid-base status of blood, despite theoretical rationale for the contrary. In the current study, we used CO tonometry to assess β in blood samples from 10 healthy volunteers, simultaneously analyzing the electrolyte shifts across the red blood cell membrane as these shifts translate the action of intracellular non-carbonic buffers to plasma. The β of the blood was re-evaluated after experimental induction of metabolic acidosis obtained by adding a moderate or high amount of either hydrochloric or lactic acid to the samples. Moreover, the impact of β and pCO on the Base excess of blood was examined. In the control samples, β was 28.0 ± 2.5 mmol/L. In contrast to the traditional assumptions, our data showed that β rose by 0.36 mmol/L for each 1 mEq/l reduction in plasma strong ion difference ( < 0.0001) and was independent of the acid used. This could serve as a protective mechanism that increases the resilience of blood to the combination of metabolic and respiratory acidosis. Sodium and chloride were the only electrolytes whose plasma concentration changed relevantly during CO titration. Although no significant difference was found between the electrolyte shifts in the two types of acidosis, we observed a slightly higher rate of chloride change in hyperchloremic acidosis, while the variation of sodium was more pronounced in lactic acidosis. Lastly, we found that the rise of β in metabolic acidosis did not induce a clinically relevant bias in the calculation of Base excess of blood and confirmed that the Base excess of blood was little affected by a wide range of pCO.
血液的非碳酸缓冲能力（β）是酸碱生理学中的一个关键概念，因为它被用于多种酸碱评估技术中，包括用于估计血液碱剩余的 Davenport 列线图和 Van Slyke 方程。到目前为止，尽管有相反的理论依据，但β一直被认为与血液的代谢酸碱状态无关。在本研究中，我们使用 CO 张力测定法评估了 10 名健康志愿者血液样本中的β，同时分析了红细胞膜上的电解质变化，因为这些变化反映了细胞内非碳酸缓冲剂对血浆的作用。在通过向样本中添加适量或大量盐酸或乳酸诱导代谢性酸中毒后，重新评估了血液的β。此外，还研究了β和 pCO 对血液碱剩余的影响。在对照样本中，β为 28.0±2.5 mmol/L。与传统假设相反，我们的数据表明，血浆强离子差每降低 1 mEq/l，β升高 0.36 mmol/L（<0.0001），且与所用酸无关。这可作为一种保护机制，增加血液对代谢性和呼吸性酸中毒组合的耐受性。钠和氯是在 CO 滴定过程中血浆浓度发生显著变化的唯一电解质。虽然在两种类型的酸中毒中电解质变化没有显著差异，但我们观察到高氯性酸中毒中氯的变化率略高，而乳酸酸中毒中钠的变化更明显。最后，我们发现代谢性酸中毒中β的升高在血液碱剩余的计算中没有引起临床相关偏差，并证实血液碱剩余受广泛范围的 pCO 影响很小。
