Crandall E D, Bidani A
J Appl Physiol Respir Environ Exerc Physiol. 1981 Feb;50(2):265-71. doi: 10.1152/jappl.1981.50.2.265.
A mathematical model has been used to study the influences of the kinetics of erythrocyte HCO3(-)/Cl-- exchange on CO2 elimination in the lung. In addition to the chloride shift, the model includes 1) CO2-H2CO3 hydration-dehydration reactions in plasma and erythrocytes; 2) CO2 reactions with hemoglobin; 3) O2 binding to hemoglobin; 4)buffering of H+ intra- and extracellularly; 5) red cell volume changes; and 6) diffusion of gases between alveoli and blood. Carbonic anhydrase activity was assumed to be available to plasma as it passes through the lung capillaries. The results show that a reduction of PHCO3(-) leads to a reduction in pulmonary CO2 elimination of up to 30%, whether or not carbonic anhydrase activity is available to plasma. Characteristic slow downstream pH and PCO2 changes predicted for each case may represent an explanation for the apparent discrepancy between in vivo and in vitro slow downstream pH changes reported previously. We conclude that red cell HCO3(-)/Cl- exchange partially limits CO2 elimination from blood in the lung and may have a major influence on capillary gas transfer when its speed is abnormally slow.
一个数学模型已被用于研究红细胞HCO3(-)/Cl-交换动力学对肺中二氧化碳清除的影响。除了氯离子转移外,该模型还包括:1)血浆和红细胞中的CO2-H2CO3水合-脱水反应;2)CO2与血红蛋白的反应;3)O2与血红蛋白的结合;4)细胞内和细胞外H+的缓冲;5)红细胞体积变化;6)肺泡与血液之间的气体扩散。假设碳酸酐酶活性在血浆通过肺毛细血管时可用。结果表明,无论血浆中是否有碳酸酐酶活性,PHCO3(-)的降低都会导致肺中二氧化碳清除率降低高达30%。每种情况下预测的特征性下游pH和PCO2缓慢变化可能解释了先前报道的体内和体外下游pH缓慢变化之间明显的差异。我们得出结论,红细胞HCO3(-)/Cl-交换部分限制了肺中血液的二氧化碳清除,当其速度异常缓慢时,可能对毛细血管气体转运产生重大影响。