Effect of early propranolol treatment in an animal model of congestive cardiomyopathy: I Mortality and Ca2+ transport in sarcoplasmic reticulum

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Abstract
Young turkeys inbred for congestive cardiomyopathy were treated with propranolol prior to the development of cardiac enlargement. One-day-old inbred and commercial turkeys received propranolol, 2 mg·kg−1.day−1 for 1 month. Propranolol-treated inbred birds showed a significantly reduced mortality from 5 to 15 days of age when compared with untreated inbred birds. However, by 28 days of age, cumulative mortality in the treated inbred birds was equal to that in the untreated inbred birds, 29 and 32%, respectively. Propranolol-treated and untreated commercial birds have a 28-day cumulative mortality of 5%. Ca2+ transport in isolated cardiac sarcoplasmic reticulum was studied at 10 and 28 days of age. At 10 days of age Ca2+ uptake and Ca2+ binding in propranolol-treated birds was reduced to 56% and 83%, respectively, of values in untreated inbred birds. By 28 days of age Ca2+ uptake and Ca2+ binding in treated and untreated inbred birds were similar. Ca2+-stimulated ATPase activity was significantly elevated in treated inbred birds compared with age-matched untreated inbred birds at 10 and 28 days of age. Ca2+ transport in isolated cardiac SR from propranolol-treated commercial control birds was not significantly different from the values in untreated commercial birds at 10 or 28 days of age. Improvement in early mortality may be due to the prevention of arrhythmias. Propranolol alters Ca2+ transport in isolated cardiac SR from inbred birds by uncoupling Ca2+-stimulated ATPase. Whether this is due to a direct effect of propranolol on the SR membrane or occurs from its beta-adrenergic blocking action is unclear.

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