Effect of ACE
Inhibitor Captopril and L-Arginine on the
Metabolism and on Ischemia-Reperfusion Injury of
the Isolated Rat Heart
J. DIVIŠOVÁ, H. VAVŘÍNKOVÁ, M. TUTTEROVÁ,
L. KAZDOVÁ, E. MESCHIŠVILI
Institute
for Clinical and Experimental Medicine, Prague,
Czech Republic
Received March 10, 2000
Accepted July 20, 2000
Summary
We investigated the effects of in vivo treatment
with the angiotensin-converting enzyme inhibitor
(ACE-I) captopril and/or of in vitro
administration of L-arginine on the metabolism
and ischemia-reperfusion injury of the isolated
perfused rat myocardium. Captopril (50 mg/l in
drinking water, 4 weeks) raised the myocardial
content of glycogen. After 25-min global
ischemia, captopril treatment, compared with the
controls, resulted in lower rates of lactate
dehydrogenase release during reperfusion
(8.58±1.12 vs. 13.39±1.88 U/heart/30 min,
p<0.05), lower myocardial lactate contents
(11.34±0.93 vs. 21.22±4.28 µmol/g d.w.,
p<0.05) and higher coronary flow recovery (by
25 %), and prevented the decrease of NO release
into the perfusate during reperfusion. In control
hearts L-arginine added to the perfusate (1
mmol/l) 10 min before ischemia had no effect on
the parameters evaluated under our experimental
conditions, presumably because of sufficient
saturation of the myocardium with L-arginine. In
the hearts of captopril-treated rats, L-arginine
further increased NO production during
reperfusion and the cGMP content before ischemia.
Our results have shown that long-term captopril
treatment increases the energy potential and has
a beneficial effect on tolerance of the isolated
heart to ischemia. L-arginine added into the
perfusate potentiates the effect of captopril on
the NO signaling pathway.
Key
words
ACE inhibitors · L-arginine · Nitric oxide ·
Cyclic GMP · Isolated rat heart ·
Ischemia-reperfusion injury
Reprint requests
J. Divišová, Institute for Clinical and
Experimental Medicine, Vídeňská 1958/9, 140 21
Prague 4, Czech Republic. Fax: 02/6108 3490
E-mail: jadi@medicon.cz
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