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-receptor blockade on energy
metabolism in rats postmyocardial infarction
Medizinische Universitätsklinik, 97080 Würzburg, Germany
Chronic treatment with 
-receptor blockers
or angiotensin-converting enzyme (ACE) inhibitors in heart failure can
reduce mortality and improve left ventricular function, but the
mechanisms involved in their beneficial action remain to be fully
defined. Our hypothesis was that these agents prevent the derangement
of cardiac energy metabolism. Rats were subjected to myocardial
infarction (MI) or sham operation. Thereafter, animals were treated
with bisoprolol, captopril, or remained untreated. Two months later,
cardiac function was measured in the isolated heart by a left
ventricular balloon (pressure-volume curves), and energy metabolism of
residual intact myocardium was analyzed in terms of total and isoenzyme
creatine kinase (CK) activity, steady-state levels (ATP,
phosphocreatine), and turnover rates (CK reaction velocity) of
high-energy phosphates (31P
nuclear magnetic resonance) and total creatine content (HPLC). Bisoprolol and partially captopril prevented post-MI hypertrophy and
partially prevented left ventricular contractile dysfunction. Residual
intact failing myocardium in untreated, infarcted hearts showed a 25%
decrease of the total, a 26% decrease of MM-, and a 37% decrease of
the mitochondrial CK activity. Total creatine was reduced
by 15%, phosphocreatine by 21%, and CK reaction velocity by 41%.
Treatment with bisoprolol or captopril largely prevented all of these
changes in infarcted hearts. Thus the favorable functional effects of
-receptor blockers and ACE inhibitors post-MI are accompanied by
substantial beneficial effects on cardiac energy metabolism.
adrenergic antagonist; angiotensin-converting enzyme inhibitors; infarction; remodeling; energy metabolism
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