• M Sair, P J Etherington, N P Curzen, C P Winlove, and T W Evans.
• Unit of Critical Care, National Heart and Lung Institute, Imperial College of Science, Technology, and Medicine, London, United Kingdom.
• Am. J. Physiol. 1996 Oct 1;271(4 Pt 2):H1620-5.

AbstractSepsis is believed to induce disturbances in microcirculatory flow and nutrient exchange, which may result in impaired tissue oxygenation. With the use of an established rat model of endotoxemia, voltametric measurements were made of skeletal muscle (tissue) oxygen tension (PtO2) and its response to inspired oxygen concentration (FIO2). Steady-state nutritive flow and the response of endotoxemic muscle to ischemia-reperfusion were also measured. In the presence of a normal arterial PO2, mean muscle PtO2 in the endotoxemic group was significantly lower than controls (52 +/- 9 vs. 24 +/- 4 Torr, P < 0.01; +/- SE). Endotoxemic muscle PtO2 values showed less heterogeneity than control groups and significant attenuation of the response to increasing FIO2 to 0.95 (mean rise in PtO2 +/- SE; 27 +/- 7 vs. 80 +/- 11 Torr for endotoxemic and control groups, respectively; P < 0.01). No steady-state differences in tissue perfusion or response to ligation-induced ischemia-reperfusion could be demonstrated between endotoxemic and control rats. These data suggest that there is significant tissue hypoxia and abnormal microvascular control of oxygenation in endotoxemia, even in the presence of normal microcirculatory perfusion.

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