Role of norepinephrine in development of short-term myocardial hibernation

Aim: 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. Conclusion:
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 antiadrenergic
treatment may be helpful for the development and sustainment of shortterm
myocardial hibernation.