The permissive role of catecholamines in the pathogenesis of hamster cardiomyopathy.
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.
D000818:Animals; D009202:Cardiomyopathies / Q000378:metabolism*; D006224:Cricetinae; D005260:Female; D006207:Half-Life; D006321:Heart / Q000294:innervation*; D008297:Male; D008647:Mesocricetus; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009336:Necrosis; D009411:Nerve Endings / Q000033:anatomy & histology*; D009638:Norepinephrine / Q000378:metabolism*
D009638:Norepinephrine