Re-evaluation of Syrian hamster Bio14.6 as a model animal for congestive heart failure and catecholamine turnover

1996 
In order to evaluate the Syrian hamster, Bio 14,6, as an animal model of congestive heart failure (CHF), the response to digitalis in its isolated cardiac muscle has been studied. Furthermore, plasma norepinephrine (NE) concentration was determined as well as myocardial NE concentration. The heart weight-to-body weight ratios were increased significantly by 19.8 and 23.8% in Stage B (20 weeks old) and Stage C (30 weeks old), respectively, compared with those of age-matched control hamsters, FIB. The pressure rate products, considered by some to be an index of cardiac work, decreased significantly in Stage B. The isolated myocardial preparation of myopathic hamsters demonstrated significant reduction in the response to ouabain at Stage B (20 weeks old). The response to NE was also inhibited in the isolated myopathic aorta. Plasma NE concentration was higher than that of control hamsters throughout of all stages. The plasma dopamine-beta-hydroxylase (DBH) activity of myopathic hamsters tended to increase with age. Myocardial tissue gradually became fibrotic with age, although the ventricular protein contents were not affected by the presence of cardiomyopathy. The NE content, whether corrected for mg protein or not, tended to decrease with age and revealed lower values than in those of FIB. At Stage C, NE content of Bio 14.6 was significantly reduced compared with that of FIB. Left ventricle dopamine (DA) concentration of Bio 14.6 maintained an almost similar level throughout all stages. The DAME ratio, which is a marker of DBH activity, tended to increase after Stage B. The cardiac tyrosine hydroxylase (TH) activity of Bio 14.6 was lower than that of control hamsters. These results confirmed the data obtained from patients with congestive heart failure, of increased plasma NE accompanied by depletion of myocardial NE content and reduction of cardiac TH activity. Bio 14.6 was recognized as an animal model of CHF both in its response to digitalis and NE turnover.
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