title: Role of norepinephrine in development of short-term myocardial hibernation.
abstract: OBJECTIVE
  To investigate the role of norepinephrine in the development of short-term myocardial hibernation.
  
  
  METHODS
  Hearts were removed from rats and set up as isometrically beating or short-term hibernation models. The hearts were perfused with modified Krebs-Henseleit buffer under a controlled perfusion pressure. The myocardial ultrastructure was examined, and the content of ATP, phosphocreatine, and glycogen in myocardium, the extent of myocyte apoptosis, and the amount of Bcl-2 and Bax products were determined after 120-min ischemia assessed by TUNEL and immunocytochemistry.
  
  
  RESULTS
  There was no significant difference between the reserpinized hearts and the NS control group with respect to heart function, myocardial ultrastructure, ATP, phosphocreatine, or glycogen content, myocyte apoptosis, or amount of Bax or Bcl-2 products. However, relative to the normal saline group, in the norepinephrine-treated hearts, heart function, and myocardial ultrastructure deteriorated significantly, apoptosis and amount of Bax product increased significantly, and the ATP, phosphocreatine, and glycogen content decreased significantly, as did the amount of Bcl-2 product.
  
  
  CONCLUSIONS
  Myocardial norepinephrine does not contribute to the development of short-term hibernation, but that exogenous NE can induce progressive decreases in coronary flow and cardiac performance, which might result from the increases in apoptosis and necrosis. Norepinephrine may be an important factor in the deterioration of myocardial structure and function during hibernation, and that anti-adrenergic treatment may be helpful for the development and sustainment of short-term myocardial hibernation.
authors.affiliation: The Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. fuzuolin@163.net
authors.forename: Zuo-lin
authors.initials: ZL
authors.lastname: Fu
authors.forename: Yi-bai
authors.initials: YB
authors.lastname: Feng
authors.forename: Hong-xia
authors.initials: HX
authors.lastname: Xu
authors.forename: Xin-ping
authors.initials: XP
authors.lastname: Zhang
authors.forename: Chun-zhi
authors.initials: CZ
authors.lastname: Shi
authors.forename: Xiang
authors.initials: X
authors.lastname: Gu
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D003326:Coronary Circulation / Q000187:drug effects; D004280:Dobutamine / Q000494:pharmacology; D006003:Glycogen / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D015425:Myocardial Reperfusion; D017682:Myocardial Stunning / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology*; D009638:Norepinephrine / Q000494:pharmacology*; D010725:Phosphocreatine / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; D010725:Phosphocreatine; D004280:Dobutamine; D000255:Adenosine Triphosphate; D006003:Glycogen; D009638:Norepinephrine