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James E. Allen, PhD; CDR C. Robert Valeri, MC

Arch Intern Med. 1974;133(1):86-96.

Abstract
Prostaglandin E_, (PGE_,) increases the deformability of red blood cells by decreasing cell volume, while PGE₂ has the opposite effect. This takes place within seconds and requires low, physiological doses of prostaglandin. They may be important in controlling capillary circulation. These effects may play a role in the evolution of shock and essential hypertension. PGE has induced sickling in susceptible cells. PGE_, inhibits while PGE₂ potentiates platelet aggregation induced by a variety of agents. These effects seem to be modulated by cyclic adenosine monophosphate levels, which are increased by PGE_, and decreased by PGE₂. Antiaggregation properties of PGE_, markedly increase the poststorage yield of functional platelets for transfusion. Erythropoiesis is stimulated both by a direct effect on erythroid precursor cells and by stimulating erythropoietin release from kidneys of animals infused with PGE₁.

Author Affiliations
Philadelphia; USNR, Chelsea, Mass

From the University of Pennsylvania School of Medicine, Philadelphia (Dr. Allen), and the Naval Blood Research Laboratory, Chelsea, Mass (Dr. Valeri).

Footnotes
Received for publication Aug 13, 1973; accepted Aug 20.

The opinions or assertions contained herein are those of the authors and are not be construed as official or reflecting the views of the Navy Department or Naval Service at large.

Reprint requests to University of Pennsylvania School of Medicine, Philadelphia 19174 (Dr. Allen).

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