Tissue oxygenation and perfusion in endotoxemia.
Sair, Mark, Philip J Etherington, Nicholas P Curzen, C Peter Winlove,
Timothy W Evans.
Unit of Critical Care, National Heart and Lung Institute, Imperial
College of Science Technology and Medicine, Dovehouse Street, London,
SW3 6LY UK, Tele/Fax: UK 0171 351 8523/4, Physiological Flow Studies
Group, Centre for Biological and Medical Systems, Imperial College of
Science Technology and Medicine, Prince Consort Road, London, SW7
2BY, UK.
APStracts 3:0186H, 1996.
Sepsis is believed to induce disturbances in microcirculatory flow and
nutrient exchange, which may result in impaired tissue oxygenation.
Utilizing an established rat model of endotoxemia, voltammetric
measurements were made of skeletal muscle 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
oxygen tension, mean muscle pTO2 in the endotoxemic group was
significantly lower than controls (mean+/-SE; 52+/-9 v 24+/-4 Torr,
p<0.01). 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
v 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.
Received 2 February 1996; accepted in final form 18 April 1996.
APS Manuscript Number H105-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 8 May 96