Klocke R A
J Appl Physiol Respir Environ Exerc Physiol. 1978 Jun;44(6):882-8. doi: 10.1152/jappl.1978.44.6.882.
Steady-state carbon dioxide excretion was studied in isolated bloodless lung preparations perfused with bicarbonate solutions. Addition of acetazolamide produced a prompt, significant decrease in the volume of excreted CO2 under all conditions studied. Excreted CO2 was derived from two sources: CO2 dissolved in the perfusate and CO2 produced by dehydration of bicarbonate in the pulmonary capillary. The relative quantity of these two sources was determined by measurement of the simultaneous excretion of acetylene. Determination of the rate of CO2 production permitted the calculation of capillary blood volume, mean capillary transit time, and the degree of catalysis of CO2 reactions by carbonic anhydrase present in the lung. Contamination of perfusate with blood carbonic anhydrase was ruled out by measuring hemoglobin concentration and carbonic anhydrase activity in pulmonary venous drainage. Comparison of steady-state CO2 production during control conditions and carbonic anhydrase inhibition indicated that bicarbonate in plasma has access to sufficient lung carbonic anhydrase to catalyze the CO2 hydration-dehydration reaction by a factor of five.
在灌注碳酸氢盐溶液的离体无血肺制备物中研究了稳态二氧化碳排泄。在所有研究条件下,加入乙酰唑胺后排出的二氧化碳量迅速且显著减少。排出的二氧化碳有两个来源:溶解在灌注液中的二氧化碳和肺毛细血管中碳酸氢盐脱水产生的二氧化碳。这两个来源的相对量通过同时测定乙炔的排泄来确定。测定二氧化碳产生速率可计算毛细血管血容量、平均毛细血管通过时间以及肺中存在的碳酸酐酶对二氧化碳反应的催化程度。通过测量肺静脉引流中的血红蛋白浓度和碳酸酐酶活性排除了灌注液被血液碳酸酐酶污染的可能性。对照条件下和碳酸酐酶抑制期间稳态二氧化碳产生的比较表明,血浆中的碳酸氢盐能够接触到足够的肺碳酸酐酶,从而使二氧化碳水合 - 脱水反应的催化效率提高五倍。