Skeletal muscle Ca2+ flux and catabolic response during sepsis
Bhattacharyya, J.; Thompson, K.D.; Sayeed, M.M.
American Journal of Physiology 265(3 Pt 2): R487-R493
1993
ISSN/ISBN: 0002-9513 PMID: 8214138 Document Number: 409293
Membrane Ca-2+ flux and net protein catabolism were studied in the skeletal muscle during experimental sepsis, Sterilized rat fecal pellets with (septic) or without (sterile) gram-negative bacteria, Escherichia coli (10-2 colony-forming units (cfu)) and Bacteroides fragilis (2 times 103 cfu), were implanted into the abdomens of male Sprague-Dawley rats (110-120 g). Septic and sterile rats were febrile and hyperlactacidemic on day 1 postimplantation. These responses subsided by day 2 in sterile but not septic rats. Initial Ca-2+ flux, estimated from measurements of 45Ca uptake by soleus muscles in vitro, was elevated on day 1 in both sterile and septic rats and on day 2 and 3 in septic rats only. The septic rat soleus muscle showed a significantly increased net protein catabolic response (measured as tyrosine release by soleus muscle, in vitro) over that found in muscles of sterile rats on day 1-3 postimplantation. The increase in Ca-2+ flux in septic (day 1-3 postimplantation) and sterile (day 1 only) rats was abolished when the rats were treated with the calcium channel blocker diltiazem. In unoperated control rat soleus muscles the Ca-2+ ionophore, ionomycin, concomitantly caused an increase in Ca-2+ flux and net protein catabolism. Overall, the present study suggested that altered cellular Ca-2+ regulation plays a role in the net protein catabolic response in the skeletal muscle during sepsis.