The evolution of -adrenergic dysfunction during the induction of canine cobalt cardiomyopathy
Autor: | Michael J. Miller, Carl V. Leier, Lorraine Gibb, Robert H. Hunsaker, Donald V. Unverferth, Richard H. Fertel, Robert L. Hamlin, James D. Thomas, Richard Croskery |
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Rok vydání: | 1984 |
Předmět: |
medicine.medical_specialty
Low protein Heart disease Physiology Cardiomyopathy Dopamine beta-Hydroxylase Catecholamines Dogs Physiology (medical) Internal medicine Receptors Adrenergic beta Heart rate medicine Animals Systole Heart Failure biology Cumulative dose Chemistry Myocardium Fissipedia Hemodynamics Heart Cobalt medicine.disease biology.organism_classification Endocrinology Heart failure Nucleotides Cyclic Cardiomyopathies Cardiology and Cardiovascular Medicine |
Zdroj: | Cardiovascular Research. 18:44-50 |
ISSN: | 0008-6363 |
DOI: | 10.1093/cvr/18.1.44 |
Popis: | This study was designed to investigate the changes in the beta adrenergic system during the induction of cobalt cardiomyopathy in dogs. Cobalt sulphate, at a dose of 5 mg·kg−1·day−1 was administered intravenously with a low protein, low thiamine diet to 13 dogs. The percentage change of the left ventricular minor axis with systole by echocardiogram (%ΔD) and dP/dtmax were used to monitor left ventricular function. Noradrenaline (NA) was measured in 24 h urine samples. Left ventricular (LV) free wall biopsies were assayed for noradrenaline (LV-NA), cyclic AMP, cyclic GMP and dopamine beta hydroxylase (LV-DBH). Lymphocytes were assayed for β-receptor density. All dogs were studied at baseline and seven were studied after a midpoint cumulative dose of 60 to 90 mg·kg−1 of cobalt; the remaining six dogs were studied when they were in heart failure and had received more than 110 mg·kg−1. During the induction of heart failure the heart rate rose from 112±6 (X±SE) at baseline to 154±9 at the midpoint and 153±9 (both P |
Databáze: | OpenAIRE |
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