Early captopril prevents myocardial infarction-induced hypertrophy but not angiogenesis

Delayed captopril, started after the healing phase of myocardial infarction, improves perfusion by reducing tissue weight without affecting the vascular capacity of the heart. Early captopril, during the healing phase, prevents reactive hypertrophy, but the effects on angiogenesis are unknown. There...

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Published inEuropean journal of pharmacology Vol. 369; no. 3; pp. 339 - 348
Main Authors Kalkman, Ed A.J, van Haren, Peter, Saxena, Pramod R, Schoemaker, Regien G
Format Journal Article
LanguageEnglish
Published Amsterdam Elsevier B.V 26.03.1999
Elsevier
Subjects
Angiotensin-Converting Enzyme Inhibitors - therapeutic use
Animals
Antihypertensive agents
Biological and medical sciences
Captopril
Captopril - therapeutic use
Cardiac metabolism
Cardiomegaly - etiology
Cardiomegaly - prevention & control
Cardiovascular system
Coronary Circulation - drug effects
Coronary flow
Coronary Vessels - pathology
Hypertrophy
Lactates - metabolism
Ligation
Male
Medical sciences
Myocardial infarction
Myocardial Infarction - complications
Myocardial Infarction - drug therapy
Myocardium - enzymology
Myocardium - metabolism
Neovascularization, Pathologic - prevention & control
Pharmacology. Drug treatments
Purines - metabolism
Rats
Rats, Wistar
Myocardial infarction
Cardiac metabolism
Captopril
Coronary flow
Hypertrophy
Heart
Infarct
Rat
Cardiovascular disease
Myocardial disease
Isolated organ
Prevention
Angiogenesis
Heart disease
Complication
Mechanism of action
Treatment efficiency
Rodentia
Metabolism
Coronary heart disease
In vitro
Vertebrata
Chemotherapy
Mammalia
Animal
Myocardium
Antihypertensive agent
ACE inhibitor
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Abstract Delayed captopril, started after the healing phase of myocardial infarction, improves perfusion by reducing tissue weight without affecting the vascular capacity of the heart. Early captopril, during the healing phase, prevents reactive hypertrophy, but the effects on angiogenesis are unknown. Therefore, the effects of early captopril (2 g/l drinking water, from 1 day until 3 weeks after myocardial infarction) on regional coronary flow related to tissue mass, were studied in isolated perfused hearts from rats, subjected to coronary artery ligation. Regional maximal vascular capacity was measured during nitroprusside-induced vasodilation, using radioactive microspheres. Maximal vascular capacity was not changed by captopril. Reactive hypertrophy in infarcted hearts only reached statistical significance in the left ventricular free wall. Since captopril prevented hypertrophy but did not affect regional capacity, peak tissue perfusion was improved. Indicating effects on metabolism, captopril restored the increased lactate/purine ratio in infarcted hearts. Thus, early captopril treatment prevented post-myocardial infarction hypertrophy but did not suppress angiogenesis, thus beneficially influencing the vascularization/tissue mass ratio, probably reflected by preservation of aerobic metabolism.
AbstractList Delayed captopril, started after the healing phase of myocardial infarction, improves perfusion by reducing tissue weight without affecting the vascular capacity of the heart. Early captopril, during the healing phase, prevents reactive hypertrophy, but the effects on angiogenesis are unknown. Therefore, the effects of early captopril (2 g/l drinking water, from 1 day until 3 weeks after myocardial infarction) on regional coronary flow related to tissue mass, were studied in isolated perfused hearts from rats, subjected to coronary artery ligation. Regional maximal vascular capacity was measured during nitroprusside-induced vasodilation, using radioactive microspheres. Maximal vascular capacity was not changed by captopril. Reactive hypertrophy in infarcted hearts only reached statistical significance in the left ventricular free wall. Since captopril prevented hypertrophy but did not affect regional capacity, peak tissue perfusion was improved. Indicating effects on metabolism, captopril restored the increased lactate/purine ratio in infarcted hearts. Thus, early captopril treatment prevented post-myocardial infarction hypertrophy but did not suppress angiogenesis, thus beneficially influencing the vascularization/tissue mass ratio, probably reflected by preservation of aerobic metabolism.
Author Saxena, Pramod R
Kalkman, Ed A.J
van Haren, Peter
Schoemaker, Regien G
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Issue 3
Keywords Myocardial infarction
Cardiac metabolism
Captopril
Coronary flow
Hypertrophy
Heart
Infarct
Rat
Cardiovascular disease
Myocardial disease
Isolated organ
Prevention
Angiogenesis
Heart disease
Complication
Mechanism of action
Treatment efficiency
Rodentia
Metabolism
Coronary heart disease
In vitro
Vertebrata
Chemotherapy
Mammalia
Animal
Myocardium
Antihypertensive agent
ACE inhibitor
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Snippet Delayed captopril, started after the healing phase of myocardial infarction, improves perfusion by reducing tissue weight without affecting the vascular...
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SubjectTerms Angiotensin-Converting Enzyme Inhibitors - therapeutic use
Animals
Antihypertensive agents
Biological and medical sciences
Captopril
Captopril - therapeutic use
Cardiac metabolism
Cardiomegaly - etiology
Cardiomegaly - prevention & control
Cardiovascular system
Coronary Circulation - drug effects
Coronary flow
Coronary Vessels - pathology
Hypertrophy
Lactates - metabolism
Ligation
Male
Medical sciences
Myocardial infarction
Myocardial Infarction - complications
Myocardial Infarction - drug therapy
Myocardium - enzymology
Myocardium - metabolism
Neovascularization, Pathologic - prevention & control
Pharmacology. Drug treatments
Purines - metabolism
Rats
Rats, Wistar
Title Early captopril prevents myocardial infarction-induced hypertrophy but not angiogenesis
URI https://dx.doi.org/10.1016/S0014-2999(99)00091-6
https://www.ncbi.nlm.nih.gov/pubmed/10225373
https://search.proquest.com/docview/69719037
Volume 369
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