Journal of Applied Physiology, Vol 77, Issue 3 1093-1100, Copyright © 1994 by American Physiological Society
Pathological O2 supply dependence of diaphragmatic and systemic O2 uptake during endotoxemia
W. S. Kim, M. E. Ward and S. N. Hussain
Critical Care Division, Royal Victoria Hospital, Montreal, Quebec, Canada.
Our aim was to assess whether endotoxemia impairs the ability of the
diaphragm to extract O2 and whether this defect leads to a greater
dependence of O2 uptake on O2 delivery. In two groups of anesthetized
mechanically ventilated dogs, the left hemidiaphragm was vascularly
isolated. Diaphragmatic blood flow and cardiac output (CO) were measured
simultaneously in all animals. Saline (S group) or Escherichia coli
endotoxin (100 mg; E group) was infused intravenously over 60 min. In both
groups, CO was reduced in stages by controlled hemorrhage, and systemic and
diaphragmatic O2 deliveries and consumptions were measured at each stage to
construct the O2 delivery-O2 consumption relationships. In the S group, the
average systemic O2 delivery below which O2 uptake became supply dependent
was 7.2 ml.kg-1.min-1. At this O2 delivery, systemic O2 extraction ratio
(ER) averaged 67.9%, whereas the maximum O2 ER was 91.3%. Critical
diaphragmatic O2 delivery and critical and maximum diaphragmatic O2 ER, by
comparison, averaged 9.0 ml.kg-1.min-1, 65%, and 81.9%, respectively.
Endotoxin infusion raised critical systemic O2 delivery to 16.7
ml.kg-1.min-1 (P < 0.05) and reduced critical and maximum systemic O2 ER
to 55.5 and 77% (P < 0.05), respectively. Similarly, critical
diaphragmatic O2 delivery in the E group increased to 14.8 ml.kg-1.min-1 (P
< 0.05), whereas critical and maximum O2 ER declined to 51.8 and 72.8%,
respectively (P < 0.05). Thus, endotoxemia impairs diaphragmatic O2
extraction. This, in turn, leads to a greater dependence of diaphragmatic
O2 uptake on O2 delivery.
