Abstract
Previous studies of chronic inflammation using the tuberculin reaction in human skin as a model have demonstrated large increases in blood flow within the lesion (Beck and Spence, 1986). This occurs in response to the increase in oxygen consumption presented by the infiltration of cells, mainly T-lymphocytes and macrophages (Gibbs et al., 1984). Despite this increase in flow, transcutaneous pO2 (tcpO2) values remain low at the centre of the reaction (Abbot et al., 1990a). Extracellular pH falls (Harrison et al., 1986), but transcutaneous pCO2 measurements rise during the course of the tuberculin reaction (Abbot et al., 1990a), indicated that the tissue acidosis was purely respiratory in origin. Thus, despite a large observed increase in O2 uptake rate (Abbot et al., 1990b) and low tissue pO2, demand does not appear to exceed the rate of oxygen delivery to the cells.
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Harrison, D.K., Abbot, N.C., Carnochan, F.M.T., Beck, J.S., James, P.B., McCollum, P.T. (1994). Protective Regulation of Oxygen Uptake as a Result of Reduced Oxygen Extraction During Chronic Inflammation. In: Vaupel, P., Zander, R., Bruley, D.F. (eds) Oxygen Transport to Tissue XV. Advances in Experimental Medicine and Biology, vol 345. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2468-7_103
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