Daniliak I G, Kogan A Kh, Sumarokov A V, Bolevich S
Ter Arkh. 1995;67(3):23-6.
30 bronchial asthma (BA) patients and 15 donors were exposed to 8.3% and 20.8% CO2 to bring out leukocytes sensitivity to CO2 by generation of active oxygen (AO) in bronchial asthma. CO2 effects on leukocyte AO generation were defined by luminol-dependent chemiluminescence (CL) before and after the exposure to CO2. It was found that in healthy subjects 8.3% and 20.8% CO2 noticeably inhibits leukocyte CL. However, in 70% of asthmatics with BA exacerbation leukocyte sensitivity to CO2 inhibition diminished. This was normal in 30% of BA patients. With BA aggravation, leukocyte sensitivity to CO2 tended to a decrease. Remission brought a complete or partial recovery of the above sensitivity. Thus, on the one hand, CO2 is involved in BA pathogenesis in terms of its inhibitory effect on AO generation by leukocytes; on the other hand, only in 30% of BA patients high CO2 concentrations as a treatment may be justified.
30名支气管哮喘（BA）患者和15名捐赠者暴露于8.3%和20.8%的二氧化碳中，通过在支气管哮喘中产生活性氧（AO）来激发白细胞对二氧化碳的敏感性。通过鲁米诺依赖的化学发光（CL）在暴露于二氧化碳之前和之后确定二氧化碳对白细胞AO生成的影响。结果发现，在健康受试者中，8.3%和20.8%的二氧化碳显著抑制白细胞CL。然而，在70%的BA加重期哮喘患者中，白细胞对二氧化碳抑制的敏感性降低。这在30%的BA患者中是正常的。随着BA加重，白细胞对二氧化碳的敏感性趋于降低。缓解使上述敏感性完全或部分恢复。因此，一方面，二氧化碳通过其对白细胞AO生成的抑制作用参与BA发病机制；另一方面，只有30%的BA患者高浓度二氧化碳作为一种治疗方法可能是合理的。
