Krintel J J, Haxholdt O S, Berthelsen P, Brøckner J
Acta Anaesthesiol Scand. 1983 Jun;27(3):252-4. doi: 10.1111/j.1399-6576.1983.tb01946.x.
Acetazolamide, an inhibitor of carbonic anhydrase, which catalyzes hydration/dehydration of carbon dioxide, has been used for correction of metabolic alkalosis in patients with chronic obstructive pulmonary disease (COPD). Animal experiments have shown that the gradient between tissue and the alveolar CO2 tension increases after inhibition of carbonic anhydrase, suggesting retention of CO2. In order to determine the true degree of carbon dioxide retention after total inhibition of carbonic anhydrase, 10 patients with COPD and pronounced metabolic alkalosis (base excess above 6) under controlled mechanical ventilation were studied. The study showed that there was a statistically significant increase in tissue PCO2 and a temporary decrease in pulmonary carbon dioxide excretion. Furthermore, it was found that PaO2 and PVO2 increased significantly after inhibition of carbonic anhydrase, which could, at least partly, explain the improvement seen in patients with COPD and metabolic alkalosis after treatment with acetazolamide.
乙酰唑胺是一种碳酸酐酶抑制剂，碳酸酐酶催化二氧化碳的水合/脱水反应，它已被用于纠正慢性阻塞性肺疾病（COPD）患者的代谢性碱中毒。动物实验表明，抑制碳酸酐酶后组织与肺泡二氧化碳张力之间的梯度增加，提示二氧化碳潴留。为了确定碳酸酐酶完全抑制后二氧化碳潴留的真实程度，对10例在控制性机械通气下患有COPD且有明显代谢性碱中毒（碱剩余超过6）的患者进行了研究。研究表明，组织PCO2有统计学意义的升高，肺二氧化碳排出量暂时减少。此外，还发现抑制碳酸酐酶后PaO2和PVO2显著升高，这至少可以部分解释COPD和代谢性碱中毒患者经乙酰唑胺治疗后病情改善的原因。
