Dm. Rosser et al., CARDIORESPIRATORY AND TISSUE OXYGEN DOSE-RESPONSE TO RAT ENDOTOXEMIA, American journal of physiology. Heart and circulatory physiology, 40(3), 1996, pp. 891-895
The dose response to-endotoxin (Escherichia coli serotype 127:B8) was
assessed in a spontaneously breathing, halothane-anesthetized, Sprague
-Dawley rat model monitoring blood pressure, aortic and renal blood fl
ows, blood gases, and bladder epithelial Po-2, a marker of organ perfu
sion. The animals received either saline or endotoxin at doses of 1, 1
0 and 100 mg/kg body wt. Blood pressure changed significantly in all t
hree endotoxin groups, though only the 100 mg/kg group showed signific
ant-changes in arterial Pco(2), arterial Po-2, and body temperature co
mpared with controls. Whereas aortic and renal blood flow rose signifi
cantly in the two lower-dose groups, an approximate one-third fall occ
urred in the 100 mg/kg group (P < 0.001). Notwithstanding these macroc
irculatory hemodynamic changes, both bladder epithelial Po-2 and arter
ial base deficit rose significantly in all groups, though only the bas
e deficit showed a progressive dose response. This model illustrates t
hat responses to-endotoxin are dose dependent but with changing patter
ns for different variables. The consistent finding of an elevated tiss
ue Po-2 in endotoxemia, regardless of dose, is suggestive of defective
cellular oxygen metabolism.