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-blocker carteolol
1 Integrated Physiology Research Laboratories, Boston University School of Medicine, Cambridge, Massachusetts 02138; 2 Whitaker Cardiovascular Institute, Boston, Massachusetts 02118; 3 Cardiac Unit, Massachusetts General Hospital, Boston, Massachusetts 02114; 4 Division of Cardiology, University of Colorado, Denver, Colorado 80262; and 5 Third Division, Department of Internal Medicine, Kyoto University, Kyoto 606, Japan
Broad-breasted
white turkey poults fed furazolidone developed dilated cardiomyopathy
(DCM) characterized by ventricular dilatation, decreased ejection
fraction, 
1-receptor density,
sarcoplasmic reticulum (SR)
Ca2+-ATPase, myofibrillar ATPase
activity, and reduced metabolism markers. We investigated the effects
of carteolol, a -adrenergic blocking agent, by administrating two
different dosages (0.01 and 10.0 mg/kg) twice a day for 4 wk to control
and DCM turkey poults. At completion of the study there was 59%
mortality in the nontreated DCM group, 55% mortality in the group
treated with the low dose of carteolol, and 22% mortality in the group
treated with the high dose of carteolol. Both treated groups showed a significant decrease in left ventricle size and significant restoration of ejection fraction and left ventricular peak systolic pressure. Carteolol treatment increased -adrenergic receptor density, and the
high carteolol dose restored SR
Ca2+-ATPase and myofibrillar
ATPase activities, along with creatine kinase, lactate dehydrogenase,
aspartate transaminase, and ATP synthase activities, to normal. These
results show that -blockade with carteolol improves survival,
reverses contractile abnormalities, and induces cellular remodeling in
this model of heart failure.
-receptor antagonist; turkey; cellular mechanisms
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