Circulation, Vol 66, 342-354, Copyright © 1982 by American Heart Association
SM Factor, T Minase, S Cho, R Dominitz and EH Sonnenblick
The cardiomyopathic Syrian hamster develops focal myocardial necrosis
beginning at 1 month of age, which leads to eventual ventricular failure
within 1 year. The pathogenesis of this myocytolytic necrosis is unknown.
Based on the nature of the cell necrosis, cytochemical evidence of vascular
alterations, and the sensitivity of the hamsters to catecholamines and
other vasoactive substances, we believe that the cardiomyopathy may be
mediated by abnormalities of the microcirculation. Nonetheless, until the
present study, no significant changes have been observed in these vessels.
To elucidate the pathogenesis of this disease, we perfused living
cardiomyopathic hamsters with silicone rubber solutions, which revealed
numerous areas of microvascular constriction, diffuse vessel narrowing and
luminal irregularity. Fixed structural lesions in these vessels could not
be demonstrated. Pretreatment of young hamsters with verapamil during the
period when they normally develop myocardial necrosis prevented
myocytolytic lesions and abolished microvascular hyperreactivity. We
believe that focal, transient spasm of small blood vessels, probably
secondary to vasoactive substances, may cause myocytolytic necrosis (a form
of reperfusion injury) in this model. This may also be a multifactorial
disease with myocellular as well as vascular abnormalities leading to
myocardial degeneration. The similarity of this disease to human and
experimental cardiomyopathy suggests that microvascular spasm may be a
common denominator of many different cardiomyopathic syndromes.
ARTICLES
Microvascular spasm in the cardiomyopathic Syrian hamster: a preventable cause of focal myocardial necrosis
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