Shapiro J I, Whalen M, Kucera R, Kindig N, Filley G, Chan L
Department of Medicine, University of Colorado Health Sciences Center, Denver 80262.
Am J Physiol. 1989 May;256(5 Pt 2):H1316-21. doi: 10.1152/ajpheart.1989.256.5.H1316.
Rats subjected to ammonium chloride-induced metabolic acidosis or respiratory acidosis caused by hypercapnia were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride induced dose-dependent systemic acidosis but did not affect intracellular brain pH. Hypercapnia caused dose-dependent systemic acidosis as well as decreases in intracellular brain pH. Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial PCO2 in both acidosis models, but it caused intracellular brain acidification in rats with ammonium chloride acidosis. Carbicarb therapy resulted in systemic alkalinization without major changes in arterial PCO2 and intracellular brain alkalinization in both acidosis models. These data demonstrate that bicarbonate therapy of systemic acidosis may be associated with "paradoxical" intracellular brain acidosis, whereas Carbicarb causes both systemic and intracellular alkalinization under conditions of fixed ventilation.
给氯化铵诱导代谢性酸中毒或高碳酸血症引起呼吸性酸中毒的大鼠，用碳酸氢钠或卡比多巴进行碱化治疗。氯化铵诱导剂量依赖性全身酸中毒，但不影响脑内细胞内pH值。高碳酸血症导致剂量依赖性全身酸中毒以及脑内细胞内pH值降低。在两种酸中毒模型中，碳酸氢钠治疗导致全身碱化和动脉血二氧化碳分压升高，但在氯化铵酸中毒的大鼠中引起脑内细胞内酸化。在两种酸中毒模型中，卡比多巴治疗导致全身碱化，动脉血二氧化碳分压无重大变化以及脑内细胞内碱化。这些数据表明，全身性酸中毒的碳酸氢盐治疗可能与“矛盾性”脑内细胞内酸中毒有关，而在固定通气条件下，卡比多巴可导致全身和细胞内碱化。
