title: Protective effects of melatonin on ischemia-reperfusion induced myocardial damage and hemodynamic recovery in rats.
abstract: OBJECTIVE
  To investigate the mechanism of melatonin (MT) protection of adult rate myocardial ischemia-reperfusion injury and its influence on rat's hemodynamic recovery.
  
  
  METHODS
  48 rats were randomly divided into MT group (n=36) and the control group (n=12), MT group was divided into three sub-groups according to different dosages: Group I (n=12) was administered with 2.5 mg/kg MT; Group II (n=12) was administered with 5 mg/kg MT; Group III (n=12) was administered with 10 mg/kg MT. The electrocardiogram of four groups was observed with the left coronary artery blocked for 10min at first and then reperfused for 15min. Hemodynamic evolving was observed and changes in energy metabolism of rat myocardium were monitored. TUNEL and immunohistochemistry were applied to detect the cell apoptosis index, protein expression of Bcl-2 and Bax.
  
  
  RESULTS
  LVDP (left ventricular developed pressure) and ± dp/dt in MT group presented better recovery at various time points than the control group. Among them, Group III had the optimal recovery degree (p < 0.05). After MT administration, ATP content in myocardial cells in MT group was significantly higher than the control group. Compared with the control group, the concentration of mitochondrial MDA and Ca2+ in myocardial cells in MT group showed a downward trend. But its GSH concentration was significantly higher than the control group (p < 0.05). The improvement degree of ATP, MDA, GSH and Ca2+ concentration in Group II over-performed Group I (p < 0.05). MT-intervened myocardial apoptosis index (AI) and Bax positive expression index declined while Bcl-2 positive expression index increased (p < 0.01).
  
  
  CONCLUSIONS
  MT effectively inhibited myocardial apoptosis during the myocardial ischemia-reperfusion of rats, protected the structural integrity of mitochondria in myocardial cells, promoted ATP synthesis, and avoided heart damage in many ways. This protection mechanism was related with anti-oxidative damage. Meanwhile, MT could promote the hemodynamic recovery after myocardial ischemia-reperfusion in rats.
authors.affiliation: Department of Obstetrics and Gynecology, the Second Affiliated Hospital of Soochow University, Suzhou, China. weipeizhucn@163.com.
authors.forename: L-F
authors.initials: LF
authors.lastname: Liu
authors.forename: Q
authors.initials: Q
authors.lastname: Qin
authors.forename: Z-H
authors.initials: ZH
authors.lastname: Qian
authors.forename: M
authors.initials: M
authors.lastname: Shi
authors.forename: Q-C
authors.initials: QC
authors.lastname: Deng
authors.forename: W-P
authors.initials: WP
authors.lastname: Zhu
authors.forename: H
authors.initials: H
authors.lastname: Zhang
authors.forename: X-M
authors.initials: XM
authors.lastname: Tao
authors.forename: Y
authors.initials: Y
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology; D002316:Cardiotonic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D006439:Hemodynamics / Q000187:drug effects* / Q000502:physiology; D008550:Melatonin / Q000494:pharmacology / Q000627:therapeutic use*; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D051381:Rats
chemical_list: D002316:Cardiotonic Agents; D008550:Melatonin