title: [The relationship between apoptosis of the cardiac myocytes and myocardial dysfunction in severely scalded rats].
abstract: OBJECTIVE
  To investigate relationship between apoptosis of the cardiac myocytes and myocardial dysfunction in severely scalded rats.
  
  
  METHODS
  Wistar rats inflicted by 40% TBSA III degree scalding were employed as the model. The myocardial tissue was obtained from the left ventricle at different postburn time points. Apoptosis was determined by the determination of myocardial tissue Caspase-3 activity and TUNEL staining (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling). The LVSP (left ventricular systolic pressure), LVEDP (left ventricular end-diastolic pressure) and +dp/dtmax (the rate of the rise of left ventricular pressure) and -dp/dtmax (the rate of the fall of left ventricular pressure) were all monitored by four-channel physiological recorder. In addition, myocardial activities of MPO and SOD were detected.
  
  
  RESULTS
  The TUNEL staining of rat myocardial cells was positive at 6 postburn hour (PBH) and reached top level at 12 PBH. The change in Caspase-3 activity was earlier than that of apoptotic morphology and reached peak values at 3 and 6 PBHs. The left ventricular function (systolic and diastolic function) was significantly impaired after the scalding and dropped to the lowest levels at 12 PBHs. The increase in myocardial tissue MPO activity was accompanied by the decrease in SOD activity.
  
  
  CONCLUSIONS
  Myocardial cellular apoptosis was one of the reasons of postburn myocardial injury in scalded rats. Caspase protease cascade pathway might be involved in the process of apoptosis, which suggested that the initiation of apoptosis was closely related to the infiltration of neutrophils and to the release of large amounts of oxygen free radicals in myocardial tissue.
authors.affiliation: Institute of Burn Research, Southwestern Hospital, The Third Military Medical University, Chongqing 400038, P.R. China.
authors.forename: Jiaping
authors.initials: J
authors.lastname: Zhang
authors.forename: Yuesheng
authors.initials: Y
authors.lastname: Huang
authors.forename: Xin
authors.initials: X
authors.lastname: Zhou
authors.forename: Jing
authors.initials: J
authors.lastname: Liu
authors.forename: Zhonghua
authors.initials: Z
authors.lastname: Luo
authors.forename: Zongcheng
authors.initials: Z
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis; D002056:Burns / Q000473:pathology* / Q000503:physiopathology*; D053148:Caspase 3; D020169:Caspases / Q000378:metabolism; D005260:Female; D008297:Male; D032383:Myocytes, Cardiac / Q000473:pathology*; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013482:Superoxide Dismutase / Q000378:metabolism; D016277:Ventricular Function, Left
chemical_list: D009195:Peroxidase; D013482:Superoxide Dismutase; C505410:Casp3 protein, rat; D053148:Caspase 3; D020169:Caspases