title: Chronic Escherichia coli infection induces muscle wasting without changing acetylcholine receptor numbers.
abstract: OBJECTIVE
  Muscle weakness in septic patients is a serious problem as it complicates and lengthens hospital stays, prolongs rehabilitation and increases costs. We examined the effects of a chronic infection with Escherichia coli on muscle function, muscle mass, and the expression of nicotinic acetylcholine receptors (AChRs).
  
  
  METHODS
  Prospective, randomized animal study in an animal laboratory, university hospital.
  
  
  METHODS
  Sprague-Dawley rats.
  
  
  METHODS
  A catheter was implanted into the external jugular vein of anesthetized rats, and a dose of 3.2x10(8) CFU of E. coli bacteria was injected; the catheter was then sealed and tunneled subcutaneously.
  
  
  RESULTS
  Animals injected with E. coli bacteria showed a significant decrease in body and muscle mass over the 14-day experimental period. Neuromuscular function was tested by mechanomyography on days 3, 7, and 14 following injection. Tetanic tension decreased over the time course of sepsis, without effecting tetanic fade. Serum levels of acute-phase protein, alpha1-acid glycoprotein, were increased by day 3, and remained significantly higher until day 14. AChRs were quantitated using 125I-labeled bungarotoxin and revealed no differences between groups.
  
  
  CONCLUSIONS
  Central venous injection of E. coli bacteria induces systemic inflammation evidenced as loss of body weight, muscle mass and increased alpha1-acid glycoprotein levels. The inflammation-induced muscle weakness is due to muscle atrophy and not to upregulated AChRs. This model may prove useful for studying maneuvers to prevent muscle wasting with inflammation.
authors.affiliation: Department of Anesthesia and Critical Care, Shriners Hospital for Children and Harvard Medical School, 51 Blossom Street, Boston, MA 02114, USA. c.frick@lrz.tu-muenchen.de
authors.forename: Christiane G
authors.initials: CG
authors.lastname: Frick
authors.forename: Heidrun
authors.initials: H
authors.lastname: Fink
authors.forename: Maria L
authors.initials: ML
authors.lastname: Gordan
authors.forename: Barbara
authors.initials: B
authors.lastname: Eckel
authors.forename: J A Jeevendra
authors.initials: JA
authors.lastname: Martyn
authors.forename: Manfred
authors.initials: M
authors.lastname: Blobner
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000818:Animals; D016470:Bacteremia / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D002405:Catheterization, Central Venous; D002908:Chronic Disease; D004195:Disease Models, Animal; D004926:Escherichia coli / Q000254:growth & development; D004927:Escherichia coli Infections / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009132:Muscles / Q000294:innervation / Q000503:physiopathology; D009133:Muscular Atrophy / Q000378:metabolism / Q000382:microbiology* / Q000503:physiopathology; D009469:Neuromuscular Junction / Q000378:metabolism / Q000503:physiopathology; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011978:Receptors, Nicotinic / Q000378:metabolism*; D018746:Systemic Inflammatory Response Syndrome / Q000378:metabolism / Q000382:microbiology / Q000503:physiopathology; D015431:Weight Loss
chemical_list: D000209:Acute-Phase Proteins; D011978:Receptors, Nicotinic