Key result
Dobutamine or norepinephrine restores LV function in dogs but increases O2 consumption and decreases mechanical efficiency.
Why the study?
Do intravenous dobutamine or norepinephrine alter myocardial oxygen consumption and mechanical efficiency in dogs with LV dysfunction?
Do intravenous dobutamine or norepinephrine alter myocardial oxygen consumption and mechanical efficiency in dogs with LV dysfunction?
Catecholamines restore contractility in LV dysfunction but at the metabolic cost of increased myocardial oxygen consumption and decreased mechanical efficiency, providing a mechanistic explanation for their deleterious effects in heart failure.
May warrant caution with catecholamines in HF for energetic costs; animal data leaves open human translation.
To investigate the metabolic cost of catecholamine use in heart failure, we administered intravenous dobutamine or norepinephrine to dogs with moderate and severe LV dysfunction until LV contractile function was restored to normal levels. Both drugs were associated with significant increases in myocardial O(2) consumption, increased coronary blood flow requirements and decreased myocardial mechanical efficiency. These mechanisms may contribute to the deleterious effects of catecholamines in heart failure.
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Nikolaidis et al. (2004) studied Heart failure / Dilated cardiomyopathy. Intravenous dobutamine or norepinephrine was evaluated on Myocardial O2 consumption, coronary blood flow requirements, and myocardial mechanical efficiency. Intravenous dobutamine or norepinephrine restored LV contractile function in dogs with LV dysfunction but significantly increased myocardial O2 consumption and decreased mechanical efficiency.
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