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(Circulation. 2002;106:e222.)
© 2002 American Heart Association, Inc.

Correspondence

Plasma Catecholamines and Chronic Congestive Heart Failure

Fuad Lechin, MD, PhD

Departamento de Ciencias Fisiologicas, Instituto de Medicina Experimental, Universidad Central de Venezuela, Caracas, Venezuela

Marcel Lechin, MD

Texas A & M University, College Station, Tex

Bertha van der Dijs, MD

Seccion de Neuroquimica y Neurofarmacologia, Instituto de Medicina Experimental, Universidad Central de Venezuela, Caracas, Venezuela

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with great interest the paper by Swedberg et al.¹ With respect to it, we will supply additional information that might aid in the understanding of the failure of imidazoline’s agonists to improve chronic congestive heart failure (CCHF) in patients.

We have assessed all plasma neurotransmitters in some 30 000 normal and diseased subjects. Included were noradrenaline (NA), adrenaline (Ad), dopamine (DA), platelet serotonin, free serotonin in the plasma, and tryptophan. These parameters were measured during supine-resting, 1-minute orthostasis, 5 minutes of moderate exercise,² and after the administration of clonidine.³ We found that the normal NA/Ad ratio >4.5. This ratio is greatly reduced in stressed mammals and severely diseased humans (<1).² With respect to the above, neural sympathetic activity (sympathetic nerves) is constituted by NA (80%) and DA (20%), whereas adrenomedullary sympathetic secretion is constituted by Ad (80%) and NA+DA (20%). Neural sympathetic activity depends on the firing rate of the locus coeruleus (LC)-NA pontine nucleus, whereas adrenomedullary sympathetic activity depends on the C1 medullary nuclei (located at the rostral ventrolateral medulla).⁴ Although both central sympathetic nuclei display associated and/or alternating activities during normal situations, dissociation of activities occurs during uncoping stress experimental situations and human diseases.⁴ Exhaustion of the LC-NA nucleus activity is the rule during these circumstances, which is reflected in deep reductions of the NA/Ad plasma ratio.⁴

All ₂ and imidazoline I₁ agonists act on the rostroventrolateral medullary area (C1) nuclei preferentially.⁵ For this reason, clonidine provokes deep reduction of plasma catecholamines and blood pressure during the . . . [Full Text of this Article]

Karl Swedberg, MD

Department of Medicine, Sahlgrenska University Hospital/Östra, Göteborg, Sweden

Michael R. Bristow, MD

Division of Cardiology, University Hospital, University of Colorado Health Sciences Center, Denver, Colo

Jay N. Cohn, MD

Cardiovascular Division, University of Minnesota Medical School, Minneapolis, Minn

Henry Dargie, MD

MRC Clinical Research Initiative in Heart Failure, University of Glasgow, Glasgow, UK

Matthias Straub, MD

Solvay Pharmaceuticals, Hanover, Germany

Curtis Wiltse, PhD; Theressa J. Wright, MD

Eli Lilly and Company, Lilly Research Laboratories, Indianapolis, Ind