Purified moniliformin does not affect the force or rate of contraction of isolated guinea pig atria

• Published in: Mycopathologia (1975) Vol. 133; no. 2; pp. 115 - 118
• Main Authors: REAMS, R. Y, THACKER, H. L, HARRINGTON, D. D, NOVILLA, M. N, WILSON, B
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer 01-01-1996
• Subjects: Animals; Biological and medical sciences; Cardiomegaly - chemically induced; Cyclobutanes - isolation & purification; Cyclobutanes - toxicity; Food toxicology; Guinea Pigs; Heart Atria; Heart Rate - drug effects; In Vitro Techniques; Male; Medical sciences; Mycotoxins - isolation & purification; Mycotoxins - toxicity; Myocardial Contraction - drug effects; Receptors, Adrenergic, beta - drug effects; Toxicology; Toxin; Atrium; Toxicity; Heart disease; Mycotoxin; Myocardium; Cardiovascular disease; Veterinary; Muscle contraction; Biological activity; Mechanism; Hypertrophy
• ISSN: 0301-486X; 1573-0832
• DOI: 10.1007/BF00439122

Chronic exposure to moniliformin results in the development of myocardial hypertrophy and degeneration. The cause of this hypertrophy is unknown. However, moniliformin-induced hypoxia or altered function of cardiac pyruvate dehydrogenase, rather than direct cardiostimulation have been proposed as potential mechanisms. Isolated guinea pig atria were used in a cumulative concentration-response model to evaluate the direct effect of moniliformin on the rate and force of atrial contraction. Moniliformin did not affect the rate or force of atrial contraction. These results are consistent with the hypothesis that moniliformin does not have a cardiostimulatory effect. Therefore cardiac stimulation. e.g. stimulation of beta-adrenergic receptors, is unlikely to be the cause of the myocardial hypertrophy observed in poultry chronically intoxicated with moniliformin.