title: Outer Balloon Ligation Increases Success Rate of Ischemia-Reperfusion Injury Model in Mice.
abstract: BACKGROUND
  Coronary artery disease is a growing public health problem and a major cause of morbidity and mortality. Experimental animal models provide valuable tools for studying myocardial ischemia reperfusion (I/R) injury in vivo.
  
  
  OBJECTIVE
  The purpose of this study was to describe a new method (outer balloon ligation) to induce myocardial I/R injury in mice.
  
  
  METHODS
  Ninety-nine male C57BL/6J mice were randomly divided into three groups: sham group, classic method group (I/R-C) and the new method group (I/R-N). The surgical procedure and recovery time were recorded. The levels of TNF-α, IL-6, cTnT and LDH were detected by ELISA kits. Hematoxylin-eosin staining was applied to assess neutrophil infiltration. Moreover, surgical survival, myocardial infarction areas, and cardiac function measurements were also recorded.
  
  
  RESULTS
  The reperfusion operation time in the I/R-N group were markedly less than the I/R-C group (14.73±2.86 vs. 168.60±33.01 sec, p <0.0001). Similarly, the recovery time in I/R-N group was shorter than the I/R-C group (45.39±15.39 vs. 101.70±19.33 min, p <0.0001). The levels of TNF-α and IL-6 in I/R-N group were also markedly lower than in I/R-C group (136.5±22.21 vs. 170.5±24.79 pg/ml, p <0.05 and 100.3±23.74 vs. 144.40±22.24 pg/ml, p <0.001). Compared I/R-N group with I/R-C group, the levels of neutrophil infiltration, cTnT and LDH had no significant differences. Surgical survival rate was 96.7% in the I/R-N group, which was significantly improved compared to the rate of 80% in the I/R-C group. However, there were no significant differences in the areas of myocardial infarction and cardiac function between the two groups.
  
  
  CONCLUSIONS
  Compared with the classic method, our new method of inducing myocardial I/R injury has higher efficiency and less tissue damage in mice, but achieves the same modeling effects.
authors.affiliation: Institute of Cardiovascular Disease, Xuzhou Medical University Xuzhou, Jiangsu, China.
authors.forename: Fengwang
authors.initials: F
authors.lastname: Hu
authors.affiliation: Department of Cardiology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.
authors.forename: Nana
authors.initials: N
authors.lastname: Zhai
authors.affiliation: Institute of Cardiovascular Disease, Xuzhou Medical University Xuzhou, Jiangsu, China.
authors.forename: Wen
authors.initials: W
authors.lastname: Gao
authors.affiliation: Institute of Cardiovascular Disease, Xuzhou Medical University Xuzhou, Jiangsu, China.
authors.forename: Pei
authors.initials: P
authors.lastname: Wu
authors.affiliation: Department of Cardiology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Luo
authors.affiliation: Department of Cardiology, the Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu, China.
authors.forename: Defeng
authors.initials: D
authors.lastname: Pan
authors.affiliation: Institute of Cardiovascular Disease, Xuzhou Medical University Xuzhou, Jiangsu, China.
authors.forename: Yang
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Institute of Cardiovascular Disease, Xuzhou Medical University Xuzhou, Jiangsu, China.
authors.forename: Dongye
authors.initials: D
authors.lastname: Li
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D015850:Interleukin-6 / Q000378:metabolism; D008026:Ligation; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology*; D009206:Myocardium / Q000473:pathology*; D009504:Neutrophils / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism / Q000473:pathology* / Q000601:surgery; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha