title: [Cardiomyocyte apoptosis and death receptor pathway in a rat model of coronary microembolization].
abstract: OBJECTIVE
  To investigate the dynamic changes of cardiomyocyte apoptosis and the role of death receptor apoptotic pathway in a rat model of coronary microembolization (CME).
  
  
  METHODS
  Adult rats were randomized to coronary microembolization (CME group, n = 63) or sham-operated group (S group, n = 55). CME model was established by aortic injection of 0.1 ml microspheres (42 microm, 3 x 10(4)/ml) into the left ventricle when the ascending aorta was temporarily clamped.S group received 0.1 ml saline injection and survived rats were randomly examined at 0, 3, 6, 12 and 24 hour post CME (n = 10 each). Heart function was evaluated by echocardiography. Myocardium sample was stained with hematoxylin-eosin and hematoxylin-basic fuchsin-picric acid to detect infarct areas. Cardiomyocyte apoptosis was detected with TUNEL staining. The expression of caspase-3 and caspase-8 was measured by Western blot analysis.
  
  
  RESULTS
  Compared with S group, the left ventricular ejection fraction was significantly decreased and left ventricular end-diastolic diameter was significantly increased in CME group (all P < 0.05) except 0 hour CME group. The infarct sizes were similar in 3 hour, 6 hour, 12 hour, and 24 hour CME groups (P > 0.05). The apoptosis index (AI) in CME group were significantly higher at each time point compared to S group (P < 0.05) except 0 hour CME group and peaked at 6 hours. Apoptotic cardiomyocytes were found mainly in the myocardial microinfarcted area and border zones. The relative expression of caspase-3 and caspase-8 in CME group were both significantly increased at 3 hours and peaked at 6 hour post CME (P < 0.05).
  
  
  CONCLUSIONS
  Cardiomyocytes apoptosis was significantly increased after coronary microembolization via activating death receptor apoptotic pathway in this coronary microembolization model.
authors.affiliation: Department of Cardiology, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, China. drlilang@163.com
authors.forename: Lang
authors.initials: L
authors.lastname: Li
authors.forename: Qiang
authors.initials: Q
authors.lastname: Su
authors.forename: Yan
authors.initials: Y
authors.lastname: Wang
authors.forename: Bo
authors.initials: B
authors.lastname: Su
authors.forename: Ri-xin
authors.initials: RX
authors.lastname: Dai
authors.forename: Yong-guang
authors.initials: YG
authors.lastname: Lu
authors.forename: Xiang-hong
authors.initials: XH
authors.lastname: Wu
authors.forename: Tang-wei
authors.initials: TW
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis; D003331:Coronary Vessels / Q000473:pathology*; D008297:Male; D032383:Myocytes, Cardiac / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D053218:Receptors, Death Domain / Q000378:metabolism*; D013923:Thromboembolism / Q000378:metabolism / Q000473:pathology*
chemical_list: D053218:Receptors, Death Domain