Journal of Applied Physiology, Vol 60, Issue 2 486-493, Copyright © 1986 by American Physiological Society
Respiratory muscle energetics during endotoxic shock in dogs
S. N. Hussain, R. Graham, F. Rutledge and C. Roussos
Respiratory muscle O2 consumption, lactate production, and endogenous
substrate utilization during endotoxic shock were assessed in two groups of
anesthetized spontaneously breathing dogs. In the endotoxin group
(Escherichia coli endotoxin 10 mg/kg iv) and the sham group (saline iv), we
sampled diaphragm, external intercostal, and gastrocnemius muscle tissue
for glycogen and lactate concentrations before and after 3 h of the
experimental period. Only in the endotoxin group did blood pressure and
cardiac output decline significantly. Arterial O2 content did not change
significantly during shock, whereas mixed venous, phrenic venous, and
femoral venous O2 contents dropped to 8.0 +/- 1.1, 5.8 +/- 0.8, and 3.6 +/-
0.6 ml/dl at 60 min of shock, respectively, with little change thereafter.
At 30 min of shock, femoral venous lactate rose higher than arterial
values, whereas at 90 min of shock, onward, phrenic venous lactate was
significantly higher than arterial concentrations. All muscle tissues
showed significant lactate production and glycogen depletion after shock.
In a second set of experiments we measured respiratory muscle blood flow
during shock with radioactive microspheres. At 60 min of shock,
diaphragmatic and intercostal blood flow rose by six- and twofold,
respectively, whereas gastrocnemius blood flow declined significantly. We
conclude that during endotoxin shock 1) the increased demands of the
respiratory muscles are met by increasing blood flow and O2 extraction; 2)
anaerobic metabolism and respiratory muscle substrate depletion, or both,
may contribute to the observed fatigue.
