Aim:To investigate the role of norepinephrine in the development of short-termmyocardial hibernation.Methods:Hearts were removed from rats and set up asisometrically beating or short-term hibernation models.The hearts were perfusedwith modified Krebs-Henseleit buffer under a controlled perfusion pressure.Themyocardial ultrastructure was examined,and the content of ATE phosphocreatine,and glycogen in myocardium,the extent of myocyte apoptosis,and the amount ofBcl-2 and Bax products were determined after 120-rain ischemia assessed by TUNELand immunocytochemistry.Results:There was no significant difference be-tween the reserpinized hearts and the NS control group with respect to heartfunction,myocardial ultrastructure,ATE,phosphocreatine,or glycogen content,myocyte apoptosis,or amount of Bax or Bcl-2 products.However,relative to thenormal saline group,in the norepinephrine-treated hearts,heart function,andmyocardial ultrastructure deteriorated significantly,apoptosis and amount of Baxproduct increased significantly,and the ATP,phosphocreatine,and glycogencontent decreased significantly,as did the amount of Bcl-2 product.Conclusion:Myocardial norepinephrine does not contribute to the development of short-termhibernation,but that exogenous NE can induce progressive decreases in coro-nary flow and cardiac performance,which might result from the increases inapoptosis and necrosis.Norepinephrine may be an important factor in the dete-rioration 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. Aim: To investigate the role of norepinephrine in the development of short-termmyocardial hibernation. Methods: Hearts were removed from rats and set up asisometrically 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 ATE phosphocreatine, and glycogen in myocardium, the extent of myocyte apoptosis, and the amount of Bcl-2 and Bax products were determined after 120-rain ischemia assessed by TUNEL and immunocytochemistry. Results: There was no significant difference be-tween the reserpinized hearts and the NS control group with respect to heartfunction, myocardial ultrastructure, ATE, phosphocreatine, or glycogen content, myocyte apoptosis, or amount of Bax or Bcl-2 products. in the norepinephrine-treated hearts, heart function, and myocardial ultrastructure deteriorated significantly, apoptosis and amount of Baxprod uct increased significantly, and the ATP, phosphocreatine, and glycogen content decreased significantly, as did the amount of Bcl-2 product. Confclusion: Myocardial norepinephrine does not contribute to the development of short-termhibernation, but that exogenous NE can induce progressive decreases in coro -nary flow and cardiac performance, which might result from the increase inapoptosis and necrosis. Norepinephrine may be an important factor in the dete-rioration 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.