Why the study?
Are myocardial concentrations of epinephrine and norepinephrine altered in diseased human hearts compared to normal hearts?
Are myocardial concentrations of epinephrine and norepinephrine altered in diseased human hearts compared to normal hearts?
Elevated myocardial epinephrine in conditions like myocardial infarction and heart failure may contribute to hypoxia and the pathogenesis of heart disease.
Suggests catecholamine imbalance contributes to pathogenesis in acute cardiac stress; leaves open therapeutic implications pending interventional studies.
Because of the exquisitely oxygen-wasting and potentially hypoxia-producing effect of epinephrine on the myocardium, its relative (compared with norepinephrine) and absolute concentration in 85 human hearts was investigated. Significant increases above normal were found in cases of fresh myocardial infarction, in congestive heart failure, and in renal uremia. It is believed that the hypoxiating action of excess epinephrine in the heart muscle constitutes an important pathogenic factor in the origin of certain forms of functional and degenerative heart disease. Prolonged illnesses of various kinds seem to reduce the myocardial norepinephrine content.
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Raab et al. (1955) studied this question.
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