Neukirch F, Verdier F, Chastang C, Fay M, Castillon du Perron M, Drutel P
Biomedicine. 1977 Dec;26(6):409-15.
Multivariate analysis of P50 changes in hypoxia, hypercapnia and polycythaemia was performed in an heterogeneous group of forty three patients: hypoxic subjects with or without hypercapnia, with or without polycythaemia and polycythaemic subjects without hypoxia. A statistical analysis was undertaken using comparison of the means, study of the correlations, principal component analysis, multiple regression and correspondence analysis. In the patients studied, P50 changes were not wholly explained by those of 2-3 DPG and pH; PaCO2, per se, did not play an important part. Haemoglobin concentration and P50 value would represent an adaptative mechanism to hypoxia: when hypoxia is moderate (80 greater than PaO2 greater than or equal to 65 torr) and isolated, oxygen haemoglobin affinity decreases (P50 increases); when hypoxia is severe (PaO2 less than 65 torr) and combined with hypercapnia and disturbed acid-base equilibrium, P50 comes back to normal range but haemoglobin increases, restoring thus, the normal blood oxygen content.
对43例异质性患者进行了低氧、高碳酸血症和红细胞增多症时P50变化的多变量分析，这些患者包括：伴有或不伴有高碳酸血症、伴有或不伴有红细胞增多症的低氧受试者，以及无低氧的红细胞增多症受试者。采用均值比较、相关性研究、主成分分析、多元回归和对应分析进行统计分析。在所研究的患者中，P50的变化不能完全由2,3-二磷酸甘油酸（2,3-DPG）和pH的变化来解释；二氧化碳分压（PaCO2）本身并不起重要作用。血红蛋白浓度和P50值可能代表了一种对低氧的适应性机制：当低氧程度较轻（80＞动脉血氧分压（PaO2）≥65托）且为单纯性时，氧合血红蛋白亲和力降低（P50升高）；当低氧严重（PaO2＜65托）且合并高碳酸血症和酸碱平衡紊乱时，P50恢复至正常范围，但血红蛋白增加，从而恢复正常的血氧含量。
