title: New experimental model of crush injury of the hindlimbs in rats.
abstract: BACKGROUND
  Crush injury (CI) remains a life-threatening condition. Because there is a shortage of animal models of CI, we purposed to develop a reproducible model of CI of hindlimbs in rats and to evaluate correlation between the volume of muscles traumatized and the severity of CI.
  
  
  METHODS
  The right or both hindlimbs of anesthetized rats were compressed for 6 hours under blocks weighing 3 kg. This was followed by 3 hours of reperfusion. Serum lactate, base excess (BE), and potassium (K) were measured at 10 minutes after cannulaton (baseline), immediately before release (compression), and 3 hours after release (reperfusion). Serum creatine phosphokinase (CK), lactate dehydrogenase (LDH), aspartate transferase (AST) and alanine transferase (ALT) were measured at baseline and reperfusion. Muscles and kidneys were evaluated morphologically. In a separate group of animals treated in the same way, survival rate was monitored for 168 hours.
  
  
  RESULTS
  Unilateral CI did not induce serious systemic impairment. Bilateral CI resulted in severe lactic acidosis. Serum K levels increased similarly and significantly in both groups. Serum CK levels correlated strongly with the volume of muscles traumatized. Bilateral CI produced a sharp increase in serum LDH, AST and ALT levels by the end of experiment. Signs of direct cellular damage and ischemia-reperfusion injury were found in histology specimens. In bilaterally crushed rats there were patent signs of acute tubular necrosis at 24 hours after insult. All rats with unilateral CI survived, whereas mortality rate reached 58.3% in rats with bilateral CI. The majority of these animals died within 24 hours after compression.
  
  
  CONCLUSIONS
  We developed a valid experimental model of severe CI of the hindlimbs in rats. Systemic responses to CI and the severity of CI appeared to correlate strongly with the volume of muscle traumatized.
authors.affiliation: Department of Traumatology, Osaka University Medical School, Osaka, Japan. pavel@hp-emerg.med.osaka-u.ac.jp
authors.forename: Pavel
authors.initials: P
authors.lastname: Akimau
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Yoshiya
authors.forename: Hideo
authors.initials: H
authors.lastname: Hosotsubo
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Takakuwa
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Tanaka
authors.forename: Hisashi
authors.initials: H
authors.lastname: Sugimoto
mesh_terms: D000136:Acid-Base Equilibrium; D000410:Alanine Transaminase / Q000097:blood; D000704:Analysis of Variance; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D001784:Blood Gas Analysis; D003402:Creatine Kinase / Q000097:blood; D003444:Crush Syndrome / Q000097:blood / Q000401:mortality / Q000503:physiopathology*; D006439:Hemodynamics; D006614:Hindlimb / Q000293:injuries*; D007770:L-Lactate Dehydrogenase / Q000097:blood; D007773:Lactates / Q000097:blood; D008297:Male; D023421:Models, Animal; D051381:Rats; D017208:Rats, Wistar; D015203:Reproducibility of Results
chemical_list: D007773:Lactates; D007770:L-Lactate Dehydrogenase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D003402:Creatine Kinase