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The protective effect and mechanism of action of the angiotensin-converting enzyme inhibitor (ACE-I) captopril was investigated in organelles from ischemic myocardial cells in a canine coronary ligation model. Sarcoplasmic reticulum (SR) and mitochondrial fractions were extracted from ischemic and nonischemic myocardial cells from captopril- and saline-treated (control) hearts. Heart rate, cardiac output, and right ventricular systolic blood pressure were similar in the captopril-treated and control groups. Left ventricular systolic blood pressure (LVPs) decreased gradually to 89% of the baseline value after captopril administration, and to 78% of the baseline value after ligation. Ca-ATPase activity in the SR, the respiratory control ratio (RCR) in the mitochondria, and dinitrophenol (DNP)-stimulated ATPase activity were significantly higher in ischemic myocardium from the captopril-treated group than from the saline-treated (control) group. The SH group content of both organelles was higher in the captopril-treated group. Our results suggest that, in addition to their hemodynamic effects, ACE-I agents containing SH groups protect the myocardium from ischemic damage by preventing enzyme oxidation.
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Hunan yi ke da xue xue bao = Hunan yike daxue xuebao = Bulletin of Hunan Medical University,
T Yanagishita, and
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August 1986,
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January 1987,
Kardiologia polska,
T Yanagishita, and
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January 1988,
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June 1984,
Kokyu to junkan. Respiration & circulation,
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April 1988,
Casopis lekaru ceskych,
T Yanagishita, and
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January 1993,
Biulleten' eksperimental'noi biologii i meditsiny,
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November 1983,
Kokyu to junkan. Respiration & circulation,
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September 1984,
Rinsho kyobu geka = Japanese annals of thoracic surgery,
T Yanagishita, and
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