Sharan M, Popel A S, Hudak M L, Koehler R C, Traystman R J, Jones M D
Centre for Atmospheric Sciences, Indian Institute of Technology, Delhi.
Ann Biomed Eng. 1998 Jan-Feb;26(1):48-59. doi: 10.1114/1.50.
Cerebral blood flow (CBF) increases as arterial oxygen content falls with hypoxic (low PO2), anemic (low hemoglobin) and carbon monoxide (CO) (high carboxyhemoglobin) hypoxia. Despite a higher arterial PO2, CO hypoxia provokes a greater increase in CBF than hypoxic hypoxia. We analyzed published data using a compartmental mathematical model to test the hypothesis that differences in PO2 in tissue, or a closely related vascular compartment, account for the greater response to CO hypoxia. Calculations showed that tissue, but not arteriolar, PO2 was lower in CO hypoxia because of the increased oxyhemoglobin affinity with CO hypoxia. Analysis of studies in which oxyhemoglobin affinity was changed independently of CO supports the conclusion that changes in tissue PO2 (or closely related capillary or venular PO2) are predictive of alterations in CBF. We then sought to determine the role of tissue PO2 in anemic hypoxia, with no change in arterial and little, if any, change in venous PO2. Calculations predict a small fall in tissue PO2 as hematocrit decreases from 55% to 20%. However, calculations show that changes in blood viscosity can account for the increase in CBF in anemic hypoxia over this range of hematocrits.
在低氧（低氧分压）、贫血（低血红蛋白）和一氧化碳（高碳氧血红蛋白）性缺氧状态下，随着动脉血氧含量下降，脑血流量（CBF）会增加。尽管动脉氧分压较高，但与低氧性缺氧相比，一氧化碳性缺氧引起的CBF增加幅度更大。我们使用隔室数学模型分析已发表的数据，以检验组织或与之密切相关的血管隔室中的氧分压差异是导致对一氧化碳性缺氧反应更大的原因这一假设。计算结果表明，由于一氧化碳性缺氧时氧合血红蛋白亲和力增加，组织而非小动脉的氧分压在一氧化碳性缺氧时较低。对氧合血红蛋白亲和力独立于一氧化碳而发生变化的研究分析支持以下结论：组织氧分压（或与之密切相关的毛细血管或静脉氧分压）的变化可预测CBF的改变。然后，我们试图确定组织氧分压在贫血性缺氧中的作用，此时动脉氧分压无变化，静脉氧分压即使有变化也很小。计算预测，当血细胞比容从55%降至20%时，组织氧分压会略有下降。然而，计算结果表明，在此血细胞比容范围内，血液粘度的变化可以解释贫血性缺氧时CBF的增加。
