AJP - Endocrinology and Metabolism, Vol 252, Issue 5 E581-E587, Copyright © 1987 by American Physiological Society
Regional blood flow and skeletal muscle energy status in endotoxemic rats
M. M. Jepson, M. Cox, P. C. Bates, N. J. Rothwell, M. J. Stock, E. B. Cady and D. J. Millward
Endotoxins induce muscle wasting in part as a result of depressed protein
synthesis. To investigate whether these changes reflect impaired energy
transduction, blood flow, O2 extraction, and high-energy phosphates in
muscle and whole-body O2 consumption (VO2) have been measured. VO2 was
measured for 6h after an initial sublethal dose of endotoxin (Escherichia
coli lipopolysaccharide 0.3 mg/100 g body wt sc) or saline and during 6h
after a second dose 24 h later. In fed or fasted rats, VO2 was either
increased or better maintained after endotoxin. In anesthetized fed rats
3-4 after the second dose of endotoxin VO2 was increased, and this was
accompanied by increased blood flow to liver (hepatic arterial supply),
kidney, and perirenal brown adipose tissue and a 57 and 64% decrease in
flow to back and hindlimb muscle, respectively, with no change in any other
organ. Hindlimb arteriovenous O2 was unchanged, indicating markedly
decreased aerobic metabolism in muscle, and the contribution of the
hindlimb to whole-body VO2 decreased by 46%. Adenosine 5'-triphosphate
levels in muscle were unchanged in endotoxin-treated rats, and this was
confirmed by topical nuclear magnetic resonance spectroscopy, which also
showed muscle pH to be unchanged. These results show that although there is
decreased blood flow and aerobic oxidation in muscle, adenosine
5'-triphosphate availability does not appear to be compromised so that the
endotoxin-induced muscle catabolism and decreased protein synthesis must
reflex some other mechanism.
