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Previous Volume 344:1711-1712 May 31, 2001 Number 22 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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For more than a century, clinicians have noted that tachycardia, cutaneous vasoconstriction, diaphoresis, and reduced urinary output are cardinal manifestations of severe heart failure and surmised that these findings are caused by increased adrenergic activity. Armed with what was then a newly developed fluorometric assay for catecholamines, our group reported in the Journal almost 40 years ago that in patients with heart failure, plasma norepinephrine concentrations are elevated,¹ whereas cardiac stores of the neurotransmitter are reduced.² We postulated that the neurotransmitter exerts a positive inotropic effect by stimulating the failing myocardium and that the vasoconstriction induced by its action helps . . . [Full Text of this Article]

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