Ritter J M, Doktor H S, Benjamin N
Department of Clinical Pharmacology, United Medical School, Guy's Hospital, London, UK.
Lancet. 1990 May 26;335(8700):1243-6. doi: 10.1016/0140-6736(90)91305-t.
The effect of an abrupt rise in bicarbonate concentration on cytoplasmic pH was studied in human platelets suspended in a Tyrode's buffer. Addition of bicarbonate raised extracellular pH but simultaneously caused pronounced cytoplasmic acidification. This effect may be due to combination of bicarbonate with hydrogen ions in extracellular fluid to form carbonic acid, which is converted by carbonic anhydrase to water and carbon dioxide. Bicarbonate ions do not diffuse rapidly across cell membranes, whereas carbon dioxide is highly diffusible and can combine with water in the cytoplasm, forming carbonic acid and reducing the intracellular pH. In accord with this explanation cytoplasmic acidification by bicarbonate was antagonised by acetazolamide (an inhibitor of carbonic anhydrase). Cytoplasmic acidification could contribute to adverse effects of intravenous sodium bicarbonate in patients with severe acidaemia. These findings add weight to the body of opinion that such treatment is both illogical and dangerous.
在悬浮于台氏缓冲液中的人血小板中，研究了碳酸氢盐浓度突然升高对细胞质pH的影响。添加碳酸氢盐会升高细胞外pH，但同时会导致明显的细胞质酸化。这种效应可能是由于碳酸氢盐与细胞外液中的氢离子结合形成碳酸，碳酸再由碳酸酐酶转化为水和二氧化碳。碳酸氢根离子不能迅速穿过细胞膜，而二氧化碳具有高度扩散性，可与细胞质中的水结合，形成碳酸并降低细胞内pH。根据这一解释，乙酰唑胺（一种碳酸酐酶抑制剂）可对抗碳酸氢盐引起的细胞质酸化。细胞质酸化可能会导致严重酸血症患者静脉注射碳酸氢钠产生不良反应。这些发现进一步支持了这样一种观点，即这种治疗既不合逻辑又危险。
