July 1956

Evaluation of the Hemostatic Properties of Synthetic Serotonin

Author Affiliations

Boston With the Technical Assistance of Nancy Martino, A.S., and Rose Mele, MT (ASCP)

From the Department of Research and the Joseph Stanton Memorial Laboratories, St. Elizabeth's Hospital, and the Department of Medicine, Tufts University Medical School, Boston. Established Investigator, American Heart Association; Associate Professor of Medicine, Tufts University School of Medicine; Director, Joseph Stanton Memorial Laboratories, and Hematologist, St. Elizabeth's Hospital (Dr. Stefanini); Damon Runyon Fellow in Cancer Research; on leave of absence from the Department of Medicine, University of Rome (Dr. Magalini).

AMA Arch Intern Med. 1956;98(1):23-27. doi:10.1001/archinte.1956.00250250029004

Introduction  Serotonin (5-hydroxytryptamine) creatinine sulfate (5-HT), a constituent of serum and platelets, has many and complex biologic functions. Some of these are connected with the mechanism of hemostasis. Thus, it is thought by many, although not proved,1 that serotonin may induce the vasoconstriction which is seen to follow vascular injury.* Also, it has been found that the parenteral administration 4 or local application5 of the drug reduces bleeding time in rabbits, while its intravenous administration 5 is stated to increase the capillary resistance in guinea pigs. Recent experiments have postulated a role of serotonin in the retraction of the clot,5 a finding which has not been confirmed.7 On the other hand, serotonin is entirely inactive in the mechanism of blood coagulation.4Allegri and Ferrari8 have recently reported control of clinical bleeding, shortening of the bleeding time, and increased capillary resistance (as judged by the

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