Cardiorespiratory and tissue oxygen dose response to rat
endotoxemia .
Rosser, D. M., R. P. Stidwill, D. Jacobson, and M Singer.
Bloomsbury Institute of Intensive Care Medicine, Department of
Medicine, University College London Medical School, 2nd Floor, Rayne
Institute Building, University Street, London WC1E 6JJ, UK
APStracts 3:0123H, 1996.
The dose response to endotoxin (E coli serotype 127:B8) was assessed
in a spontaneously breathing, halothane anesthetised, Sprague-Dawley
rat model monitoring blood pressure, aortic and renal blood flows,
blood gases and bladder epithelial PO2, a marker of organ perfusion.
The animals received either saline or endotoxin at doses of 1mg, 10mg
and 100mg per kg body weight. Blood pressure changed significantly in
all three endotoxin groups though only the 100mg/kg group showed
significant changes in PaCO2, PaO2 and body temperature compared to
controls. Whereas aortic and renal blood flow rose significantly in
the two lower dose groups an approximate one-third fall occurred in
the 100mg/kg group (p<0.001). Notwithstanding these
macrocirculatory hemodynamic changes, both bladder epithelial PO2 and
arterial base deficit rose significantly in all groups though only
the base deficit showed a progressive dose response. This model
illustrates that responses to endotoxin are dose dependent but with
changing patterns for different variables. The consistent finding of
an elevated tissue PO2 in endotoxemia, regardless of dose, is
suggestive of defective cellular oxygen metabolism.
Received 14 December 1995; accepted in final form 6 March 1996.
APS Manuscript Number H1169-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 27 March 96