Blood flow and plasma extravasation in skeletal muscle during endotoxemia. A study in rats

Apparently skeletal muscle is little affected during endotoxemia. We therefore studied in anesthetized rats the effects of endotoxin on blood flow and extravasation of plasma in skeletal muscle of different regions (thorax, abdomen, foreleg, hind limb) and whether or not extravasation, if present, is related to hypoperfusion. Endotoxemia was induced by infusion of E. coli endotoxin (10 mg/kg) from t = 0 to t = 60 min (E-group: n = 8); control rats received saline (C-group: n = 8). One femoral artery (C:n = 6, E: n = 6) was ligated to cause muscle hypoperfusion in that limb. Experiments ended at t = 120 min. Cardiac output and blood flow were measured at t = 0 and 120 (radioactive microspheres); extravasation was measured with a double isotope technique: 125I-HSA as plasma and 51Cr-labeled red cells as intravascular marker (injected at t = -50 and t = -40 min, respectively). Cardiac output decreased and lactate levels increased markedly during endotoxemia, but muscle blood flow was not affected: percentage of cardiac output to muscles increased in all regions (by 50-100%, p less than 0.05). Femoral artery ligation caused a 33% decreased in muscle blood flow at t = 0; at t = 120 the reduction was 88% in the E-, but only 15% in the C-group. Extravasation of 125I-HSA (from t = 0 to t = 120, as percentage of the total integrated plasma supply over 2-hr) increased during endotoxemia for abdominal, thoracic and foreleg muscles by 178, 148 and 133%, respectively (p less than 0.05). In the non-ligated hind limb endotoxin had no significant effect on extravasation; hypoperfusion alone caused a 300% increase (p less than 0.05%) and the combined effect was a 400% increase (p less than 0.05) in extravasation. Our results show that during endotoxemia muscle blood flow hardly decreases, and that plasma extravasation is only substantial when muscle blood flow is also severely impaired.