The evolution of -adrenergic dysfunction during the induction of canine cobalt cardiomyopathy

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Abstract
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−1 at baseline to 254±46 kPa·s−1 (P−1 (P−1 tissue at baseline to 48±8 pg·mg−1 at the midpoint and 47± 15 pg·mg−1 at the final measurement (both P<0.05). The density of peripheral lymphocyte beta receptors also fell significantly while the ratio of myocardial cyclic AMP/cyclic GMP fell from 243 ±56 at baseline to 60± 12 (P<0.01) at the midpoint and 46±8 (P<0.01) at the final measurement. These data indicate that aberrations in beta adrenergic function inhibit vital support mechanisms to the cardiovascular system during heart failure.
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