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Serotonin Concentrations and Hemodynamic Studies

ARNOLD ADICOFF, MD; CARL S. ALEXANDER, MD, PhD; RICHARD B. DAVIS, MD

Arch Intern Med. 1966;117(2):250-255.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

SINCE the early descriptions of the carcinoid syndrome,^1-4 it has been assumed that the associated hyperserotonemia is responsible for the symptoms and development of the cardiac lesions. These lesions, which appear mainly on the right side of the heart, are characterized by subendocardial proliferation of fibrous tissue resulting in thickening of the endocardium and chordae tendineae with thickening and distortion of the tricuspid and pulmonic valves. Relative sparing of the left side of the heart has been attributed to the inactivation of free serotonin by monamine oxidase present in the lungs.⁵ However, all but two of the studies of serotonin levels in pulmonary arterial and systemic arterial blood,^6-11 reported no significant differences across the pulmonary vascular bed. Goble⁸ and Welti¹⁰ noted serotonin levels in the pulmonary artery significantly greater than in the brachial artery. This finding has not been confirmed by other investigators, but is often cited as evidence for . . . [Full Text PDF of this Article]

Author Affiliations
MINNEAPOLIS

From the departments of medicine, Minneapolis Veterans Hospital and University of Minnesota Medical School, Minneapolis.

Footnotes
Received for publication July 8, 1965; accepted Sept 14.

Reprint requests to Cardiovascular Section, Veterans Hospital, Minneapolis, Minn 55417 (Dr. Adicoff).

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