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The permissive role of catecholamines in the pathogenesis of hamster cardiomyopathy
Insights
Norepinephrine (NE) nerve endings proliferate during heart necrosis in cardiomyopathic hamsters. Increased NE uptake and turnover suggest NE promotes heart damage in this hereditary cardiomyopathy.
Area of Science:
- Cardiology
- Neuroscience
- Pathology
Background:
- Beta-adrenergic blockers show protective effects in cardiomyopathic hamsters.
- The role of catecholamines in hereditary cardiomyopathy requires further investigation.
Purpose of the Study:
- To investigate the role of catecholamines in hamster hereditary cardiomyopathy pathogenesis.
- To visualize ventricular adrenergic nerve terminals and determine norepinephrine (NE) uptake and turnover.
Main Methods:
- Fluorescence histochemistry to visualize adrenergic nerve terminals.
- Intravenous injection of labeled NE to measure uptake and turnover.
- Analysis of NE nerve endings in relation to myocardial lesions.
Main Results:
- Proliferation of fluorescent nerve endings correlated with heart necrotic changes.
- Increased NE uptake and elevated elimination rate constant observed during the necrotic stage.
- NE nerve endings were absent in the terminal disease stage.
Conclusions:
- Norepinephrine (NE) turnover is linked to the progression of hamster hereditary cardiomyopathy.
- NE appears to play a permissive role in promoting heart necrotic changes in this disease model.
Abstract:
It was previously shown that beta-adrenergic blockers exert a protective action on the development of heart necrotic changes in cardiomyopathic hamsters. To further investigate the possible role of catecholamines in the pathogenesis of the hamster hereditary cardiomyopathy, the ventricular adrenergic nerve terminals were visualized by fluorescence histochemistry, and NE uptake and turnover were determined after i.v. injection of labeled NE. It was found that the fluorescent nerve endings strongly proliferate with the occurrence of heart necrotic changes. With healing of the myocardial lesions, the difference between control and myopathic hearts is less apparent, and NE nerve endings are literally absent in the terminal stage of the disease. There was a marked increase in NE uptake during the necrotic stage and, at the same time, a considerable rise in elimination rate constant with a maximum level at terminal state, suggesting that the NE turnover is related to the progression of the disease. In light of the present findings, it can be surmised that NE plays a permissive role in the genesis of the hamster disease by promoting the heart necrotic changes.