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Myocardial metabolism of cyclic 3,5‐adenosine monophosphate as influenced by dipyridamole and theophylline in patients with coronary heart disease
Author(s) -
Hombach V.,
Behrenbeck D. W.,
Tauchert M.,
GilSanchez D.,
Jansen W.,
Hötzel J.,
Niehues B.,
Hilger H. H.
Publication year - 1979
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960020608
Subject(s) - dipyridamole , medicine , theophylline , aminophylline , adenosine , cardiology , hemodynamics , angina , heart rate , blood flow , coronary steal , cyclic adenosine monophosphate , ischemia , endocrinology , anesthesia , blood pressure , myocardial ischemia , myocardial infarction , receptor
Abstract In a total of 16 individuals, 4 females and 12 male patients ranging from 36 to 54 years, with proven coronary heart disease, hemodynamic parameters and coronary blood flow (argon method) were measured at rest and after administration of dipyridamole, 0.5 mg/kg body weight, and theophylline, 0.24 g i.v. Simultaneously, blood samples were taken from the arterial and coronary venous blood for determinations of oxygen content and concentrations of cyclic 3,5‐adenosine monophosphate (cAMP) and lactate. Thus, myocardial oxygen consumption and uptake or release of cAMP and lactate could be calculated according to the Fick principle. After administration of dipyridamole, heart rate and cardiac index slightly increased together with a decrease in arterial pressure. Myocardial blood flow significantly increased, whereas myocardial oxygen consumption remained unchanged during the dipyridamole period. In nine patients myocardial release of cAMP and lactate could be observed during the dipyridamole action, whereas in the remaining seven patients there were only insignificant changes of release or uptake of cAMP and lactate in the dipyridamole and theophylline periods. Six of nine patients in the first group revealed specific anginal complaints corresponding to the release of cAMP and lactate, whereas only two patients in the non‐cAMP‐releasing individuals had characteristic angina pectoris. These data suggest that dipyridamole may induce myocardial ischemia with anginal complaints and that, under certain circumstances, myocardial release of cAMP as well as lactate might serve as biochemical correlates of these ischemic conditions.

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