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Abstract
The morphologic-functional correlative studies that we have carried out in the past
25 years with the various catecholamines have served as an example for analyzing myocardial
reaction patterns and the reactions of the cardiac muscle cells to insult. These studies
disclosed the unique nature of isoproterenol in producing 'infarct-like' myocardial
necrosis. It appears that the pathogenesis of the catecholamine-induced myocardial
necrosis is multifactorial. Our early studies suggested the role of relative hypoxia.
Later studies by using extracellular fine structural protein tracers demonstrated
the importance of microcirculatory effects as well as, in the norepinephrine model,
that of early sarcolemmal membrane permeability alteration. The Ca2+ overload theory
is supported not only by the experimental observations but also by its successful
application in clinical cardiology. A new contribution is the recognition of catecholamine
oxidation products in producing myocardial injury. Experimental data indicate that
catecholamines play an important role in reperfusion and ischemic myocardial injuries.
The sequence of events demonstrated by our studies with catecholamines might represent
a common pathway in the evolution of myocardial changes in humans who develop myocardial
lesions without narrowing or obstruction of coronary arteries. Investigation in the
field of molecular and cellular cardiology has led to a better understanding of current
clinical problems and helped to devise procedures for the prevention and management
of human myocardial disorders. The isoproterenol-induced myocardial necrosis served
as model to Professor A. Fleckenstein to formulate the Ca2+ overload theory of myocardial
injury and develop a series of now widely used Ca2+ antagonistic drugs for the management
and the prevention of human myocardial diseases.