title: [Cardioprotection of testosterone in rat hearts subjected to ischemia/reperfusion].
abstract: OBJECTIVE
  To investigate the chronic cardioprotection of testosterone against ischemia/reperfusion injury and acute effect against H2O2-stress injury.
  
  
  METHODS
  The vas deferens were ligated bilaterally and the testes removed from male Sprague-Dawley rats, and testosterone propionate was supplemented every day. Eight weeks after gonadectomy, all the hearts were mounted on a Langendorff apparatus to assess the level of lactate dehydrogenase (LDH) in the coronary effluent and the infarct size. Isolated adult ventricular myocytes were obtained by enzymatic dissociation, in which H2O2-stress injury model was copied. The myocyte contraction was determined, and mitochondrial reactive oxygen species (ROS) production was measured by loading with fluorescent probe DCFH-DA.
  
  
  RESULTS
  In gonadectomy model, pretreatment with testosterone propionate significantly decreases the LDH release and the infarct size. In the isolated myocytes model, testosterone attenuated the decreases of +/- dL/dtmax and dL which produced by H2O2-stress, and prevented the production of ROS induced by H2O2-stress. Co-treatment with atractyloside or 5-HD attenuated the effect of testosterone.
  
  
  CONCLUSIONS
  The findings show the chronic cardioprotection of testosterone against ischemia/reperfusion injury and acute effect against H2O2-stress injury via opening of mitoK(ATP) channel or/and the inhibiting mitochondrial permeability transition pore.
authors.affiliation: Department of Physiology, Zhejiang Medical College, Hangzhou 310053, China.
authors.forename: Jue
authors.initials: J
authors.lastname: Wang
authors.forename: Bo
authors.initials: B
authors.lastname: Yang
authors.forename: Qin
authors.initials: Q
authors.lastname: Gao
authors.forename: Qiang
authors.initials: Q
authors.lastname: Xia
mesh_terms: D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D006861:Hydrogen Peroxide; D054086:KATP Channels / Q000378:metabolism; D008297:Male; D033681:Mitochondrial Membrane Transport Proteins / Q000187:drug effects; D000083162:Mitochondrial Permeability Transition Pore; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D009919:Orchiectomy; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013739:Testosterone / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D002316:Cardiotonic Agents; D054086:KATP Channels; D033681:Mitochondrial Membrane Transport Proteins; D000083162:Mitochondrial Permeability Transition Pore; D013739:Testosterone; D006861:Hydrogen Peroxide