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

Weiyang Wang, Ken Okamoto, Danny O. Jacobs

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)951-961
Number of pages11
JournalJournal of Trauma
Volume52
Issue number5
StatePublished - 2002
Externally publishedYes

Fingerprint

Intra-Articular Fractures
Calcaneus
Serum
Endotoxins
Complement Activation
Lipopolysaccharides
Zymosan
Punctures
Ligation
Muscles
Complement Receptors
Sepsis
Homeostasis
Sodium
Complement System Proteins
Hot Temperature

Keywords

  • Complement activation
  • Complement membrane attack complex
  • Critical care
  • Lipopolysaccharide
  • Potassium
  • Septic shock
  • Skeletal muscle
  • Sodium
  • Zymosan

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine

Cite this

Open reduction and internal fixation of displaced intra-articular fractures of the calcaneus. / Wang, Weiyang; Okamoto, Ken; Jacobs, Danny O.

In: Journal of Trauma, Vol. 52, No. 5, 2002, p. 951-961.

Research output: Contribution to journalArticle

Wang, W, Okamoto, K & Jacobs, DO 2002, 'Open reduction and internal fixation of displaced intra-articular fractures of the calcaneus', Journal of Trauma, vol. 52, no. 5, pp. 951-961.
Wang, Weiyang ; Okamoto, Ken ; Jacobs, Danny O. / Open reduction and internal fixation of displaced intra-articular fractures of the calcaneus. In: Journal of Trauma. 2002 ; Vol. 52, No. 5. pp. 951-961.
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abstract = "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.",
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AU - Wang, Weiyang

AU - Okamoto, Ken

AU - Jacobs, Danny O.

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N2 - 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.

AB - 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.

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