SKELETAL-MUSCLE CA-2+ FLUX AND CATABOLIC RESPONSE DURING SEPSIS

Membrane Ca2+ flux and net protein catabolism were studied in the skel etal muscle during experimental sepsis. Sterilized rat fecal pellets w ith (septic) or without (sterile) gram-negative bacteria, Escherichia coli [10(2) colony-forming units (cfu)] and Bacteroides fragilis (2 X 10(3) cfu), were implanted into the abdomens of male Sprague-Dawley ra ts (110-120 g). Septic and sterile rats were febrile and hyperlactacid emic on day 1 postimplantation. These responses subsided by day 2 in s terile but not septic rats. Initial Ca2+ flux, estimated from measurem ents of Ca-45 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 onl y. The septic rat soleus muscle showed a significantly increased net p rotein catabolic response (measured as tyrosine release by soleus musc le, in vitro) over that found in muscles of sterile rats on day 1-3 po stimplantation. The increase in Ca2+ flux in septic (day 1-3 postimpla ntation) and sterile (day 1 only) rats was abolished when the rats wer e treated with the calcium channel blocker diltiazem. In unoperated co ntrol rat soleus muscles the Ca2+ ionophore, ionomycin, concomitantly caused an increase in Ca2+ flux and net protein catabolism. Overall, t he present study suggested that altered cellular Ca2+ regulation plays a role in the net protein catabolic response in the skeletal muscle d uring sepsis.