The Journal of Thoracic and Cardiovascular Surgery, Vol 92, 425-433, Copyright © 1986 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association
Protective metabolic effects of propranolol during total myocardial ischemia
CD Veronee, WR Lewis, MW Takla, EA Hull-Ryde and JE Lowe
Clinical trials have shown an increase in survival in patients treated with
beta blockers after infarction. In addition, the majority of patients
undergoing myocardial revascularization are also treated preoperatively
with beta blockers. It is commonly thought that beta blockers exert their
protective effect primarily by decreasing heart rate and subsequent
myocardial work. The present study was designed to determine whether beta
blockade has any primary protective metabolic effects on globally ischemic
myocardium. Thirty-four anesthetized dogs underwent total myocardial
ischemia at 37 degrees C. High-energy nucleotide and lactate levels in left
ventricular tissue samples were determined at control and at 15 minute
intervals as well as at the onset of ischemic contracture in 24 dogs.
Seventeen dogs were treated with propranolol before ischemia. The time to
ischemic contracture in control dogs was 63.3 +/- 1.4 minutes compared with
75.9 +/- 2.2 minutes in the propranolol-treated group (p less than 0.01).
In addition to significantly delaying the onset of ischemic contracture,
propranolol also decreased the rate of anaerobic glycolysis during
ischemia. Ischemic contracture occurred in the control group with an
average adenosine triphosphate level of 1.26 +/- 0.08 mumol compared to
0.91 +/- 0.08 mumol/gm wet weight for the beta blocked group (p less than
0.0025). These are the first data suggesting that the protective effects of
beta blockade may be related to a beneficial effect on ischemic myocardial
metabolism allowing myocardium to survive with lower levels of adenosine
triphosphate.
