title: [Study on the pathogenesis of stress myocardial injury].
abstract: OBJECTIVE
  To investigate  the  pathogenesis of stress myocardial  injury.
  
  
  METHODS
  Thirty Wistar rats were randomly divided into three groups, with 10 rats in each group: normal control group, movement restriction and ice swimming stress group (rat movement was restricted 6 hours per day; beginning from 13th day rats were allowed to swim in ice water for 5 minutes, ice stress group), and endotoxin stress group [intraperitoneal injection of lipopolysaccharide (LPS) 10 mg/kg, LPS group]. The myocardial tissue was harvested, the pathological changes in myocardial was observed with light microscopy, and the changes in myocardial ultrastructure were observed with electron microscope. The levels of serum cardiac troponin I (cTnI) was determined by enzyme-linked immunosorbent assay (ELISA), apoptosis of myocardial cells was detected by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), and the apoptotic index was calculated.The caspase-8 and caspase-3 expression in myocardial tissue were assessed by immunohistochemistry. The correlation between caspase and apoptotic index was analyzed.
  
  
  RESULTS
  Compared with normal control group, in ice stress group and LPS group, myocardial tissue was found to be injured seriously in different degrees under light microscopy and electron microscopy; the content of cTnI (μg/L) in serum was significantly increased (0.63 ± 0.12, 0.74 ± 0.08  vs.  0.53 ± 0.03, P < 0.05 and P < 0.01); apoptosis index of myocardial tissue was significantly increased in different degrees [(7.91 ± 1.71)%, (12.94 ± 2.00)%  vs.  0]; caspase-8 and caspase-3 expressions in the myocardium were increased (caspase-8 gray scale: 126.65 ± 3.13, 114.82 ± 8.67  vs.  156.99 ± 9.66; caspase-3 gray scale: 130.20 ± 2.96, 108.58 ± 5.72  vs.  160.51 ± 5.25, all P < 0.01). However, the above indexes in LPS group were significantly higher than those in ice stress group (P < 0.05 or P < 0.01). The correlation analysis showed that in ice stress group, positive correlation was found between caspase-8, caspase-3 and apoptotic index [r(1) = 0.914, P(1) = 0.002; r(2) = 0.929, P(2) = 0.001]; in LPS group, the positive correlation also exist between caspase-8, caspase-3 and apoptotic index [r(1) = 0.956, P(1) = 0.000; r(2) = 0.916, P(2) = 0.001].
  
  
  CONCLUSIONS
  Severe stress may produce stress injury of myocardium via increasing expression of caspase-8 and caspase-3 protein.
authors.affiliation: Intensive Care Unit, Affiliated Hospital of Inner Mongolia Medical College, Huhehot 010050, Neimenggu, China.
authors.forename: Jing
authors.initials: J
authors.lastname: Lin
authors.forename: Li-hua
authors.initials: LH
authors.lastname: Zhou
authors.forename: Xin
authors.initials: X
authors.lastname: Chen
authors.forename: Zhi-min
authors.initials: ZM
authors.lastname: Huang
authors.lastname: Asileng
mesh_terms: D000818:Animals; D017209:Apoptosis; D053148:Caspase 3 / Q000378:metabolism; D053181:Caspase 8 / Q000378:metabolism; D004195:Disease Models, Animal; D004731:Endotoxins / Q000009:adverse effects; D008297:Male; D032383:Myocytes, Cardiac / Q000378:metabolism* / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological; D054549:Takotsubo Cardiomyopathy / Q000378:metabolism* / Q000473:pathology; D019210:Troponin I / Q000097:blood
chemical_list: D004731:Endotoxins; D019210:Troponin I; C505410:Casp3 protein, rat; C505528:Casp8 protein, rat; D053148:Caspase 3; D053181:Caspase 8