An ischemic canine limb model was used to determine whether endotoxin reduces the ability of resting skeletal muscle to extract O2 and whether increasing the arterial P(O2) would increase its O2 extraction. Isolated limbs were pump perfused via an extracorporeal circuit with membrane oxygenator at three progressively lower flows and P(O2) of both 60 and 200 Torr, whereas the rest of the body remained normoxic and normotensive. Six anesthetized, paralyzed dogs were injected with endotoxin (4 mg/kg, ENDO), and another six were controls (CONT). Limb critical O2 delivery was higher (P<0.05) in ENDO than CONT (8.3 vs. 6.1 ml·kg-1·min-1). Critical venous P(O2) was also higher (P<0.05) in ENDO than CONT (38 vs. 30 Torr). Critical O2 extraction ratio was lower (P<0.05) in ENDO than CONT (0.60 vs. 0.73). There were no differences in these variables between low and high arterial P(O2). We concluded that 1) endotoxin can cause a small but significant O2 extraction defect in skeletal muscle, 2) increasing arterial P(O2) did not correct such a defect, nor did it improve O2 uptake in ischemic, but otherwise healthy, muscle, and 3) skeletal muscle may contribute to the peripheral O2 extraction defect in adult respiratory distress syndrome insofar as endotoxin effects model those found in adult respiratory distress syndrome.
ASJC Scopus subject areas
- Physiology (medical)