Patients with the adult respiratory distress syndrome (ARDS) show a pathological dependence of O2 consumption (V̇O2) on O2 delivery (Q̇O2, blood flow x arterial O2 content). In these patients, a defect in tissues' ability to extract O2 from blood can leave tissue O2 needs unmet, even at a normal Q̇O2. Endotoxin administration produces a similar state in dogs, and we used this model to study mechanisms that may contribute to human pathology. We measured systemic and hindlimb V̇O2 and Q̇O2 while reducing cardiac output by blood withdrawal. At the onset of supply dependence, the systemic Q̇O2 was 11.4 ± 2.7 ml · kg-1 · min-1 in the endotoxin group vs. 8.0 ± 0.7 in controls (P < 0.05). At this point, the endotoxin-treated animals extracted only 61 ± 11% of the arterial O2, whereas control animals extracted 70 ± 7% (P < 0.05). Systemic V̇O2 rose by 15% after endotoxin (P < 0.05) but did not change in controls. Despite this poorer systemic ability to extract O2 by the endotoxin-treated dogs, isolated hindlimb O2 extraction at the onset of supply dependence was the same in endotoxin-treated and control dogs. At normal levels of Q̇O2 hindlimb V̇O2 in endotoxin-treated dogs was 23% higher than in controls (P < 0.05). Fractional blood flow to skeletal muscle did not differ between control and endotoxin-treated dogs. Thus skeletal muscle was not overperfused in endotoxemia and did not contribute to a systemic extraction defect by stealing blood flow from other tissues. Skeletal muscle in endotoxin-treated dogs demonstrated an increase in V̇O2 but no defect in O2 extraction, differing in both respects from the intestine.
ASJC Scopus subject areas
- Physiology (medical)