Open reduction and internal fixation of displaced intra-articular fractures of the calcaneus

Background Inappropriate complement activation is closely related to tissue injury and organ dysfunction during systemic infection. It is not clear, however, if endotoxin-induced complement activation is responsible for changes in myocellular sodium homeostasis during sepsis. Methods Rats underwent cecal ligation and puncture (CLP) or sham operation. Twenty-four hours after operation, fast-twitch extensor digitorum longus (EDL) muscles were isolated, incubated at 30°C for 1 hour in Krebs-Henseleit buffer (KHB) (pH 7.4), and used to measure intracellular Na⁺ and K⁺ contents. Blood samples were collected to measure serum hemolytic complement activity and endotoxin levels. In addition, EDL muscles isolated from normal animals were incubated at 30°C for 1 hour with zymosan-activated (10 mg/mL at 37°C for 1 hour) rat sera, with lipopolysaccharide (LPS)-activated (LPS from Escherichia coli 055;B5, 10 or 200 μg/mL at 37°C for 30 minutes) rat sera, with heat-inactivated (56°C for 30 minutes) rat sera, with LPS (1 or 20 μg/mL), or in KHB. EDL muscles isolated from normal animals were also incubated with septic sera collected 6 or 24 hours after CLP with or without administration of soluble complement receptor type 1 (20 mg/kg, intraperitoneally). Myocellular Na⁺ and K⁺ contents ([Na⁺]_i and [K⁺]_i) were assayed using “washout” technique. Soluble C5b-9 complex levels in zymosan-activated or LPS-activated human sera were determined by enzyme-linked immunosorbent assay to evaluate the degree of complement activation induced by zymosan or LPS. Results Myocellular [Na⁺]_i and [Na⁺]_i/[K⁺]_i ratios increased significantly 24 hours after CLP as compared with sham operation and were associated with decreased serum hemolytic complement activity and increased serum endotoxin levels. Zymosan-activated rat sera at sublytic concentrations markedly increased [Na⁺]_i and [Na⁺]_i/[K⁺]_i ratios in isolated EDL muscles relative to heat-inactivated rat sera. LPS-activated rat sera, however, did not alter these two indices. In addition, myocellular [Na⁺]_i and [Na⁺]_i/[K⁺]_i ratios were equivalent among normal EDL muscles incubated with septic sera, soluble complement receptor type 1-treated septic sera, or KHB. Conclusion These results collectively suggest that polymicrobial sepsis, as produced by CLP, alters sodium homeostasis in fast-twitch skeletal muscles in association with changes in systemic complement activation and circulating endotoxin levels. Although endotoxin can activate the complement cascade, endotoxin-induced complement activation does not appear to be responsible for changes in myocellular sodium homeostasis observed during sepsis in rats.