Abstract
The factors which affect O2 uptake by whole the body or by organs such as skeletal muscles have been extensively studied. Some of these studies have shown that O2 uptake (VO2) may be altered by changes in blood flow (Q) [1, 2], arterial oxygen tension (PaO2) [1,2], other blood gas parameters (O2 capacity [3], O2 hemoglobin affinity [4–7], or by saturation of the mitochondrial ATP-generating capacity [8]. However, in normal conditions, when O2 demand is low, it is generally admitted that O2 uptake is independent of these parameters [2]. More generally, O2 uptake is independent of O2 delivery until very low levels of O2 delivery are reached [9-11]. When O2 demand is high, tissue O2 uptake becomes O2 delivery-limited over a wider range. Recently, some experimental data in canine skeletal muscle have demonstrated that in situations of high O2 demand, O2 uptake can be limited not only by O2 delivery but also by O2 diffusion [12, 13]. In addition, certain pathological states such as adult respiratory distress syndrome and sepsis have been found to alter drastically the relationships between O2 delivery and O2 uptake [14–16].
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Vicaut, E., Duvelleroy, M. (1991). Determining Factors of Tissue O2 Uptake. In: Dhainaut, JF., Payen, D. (eds) Strategy in Bedside Hemodynamic Monitoring. Update in Intensive Care and Emergency Medicine, vol 11. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-84167-5_4
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DOI: https://doi.org/10.1007/978-3-642-84167-5_4
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