This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by LICHTMAN, M. A. Articles by WHITBECK, A. A. Search for Related Content PubMed PubMed Citation Articles by LICHTMAN, M. A. Articles by WHITBECK, A. A.

(Circulation. 1974;49:881.)
© 1974 American Heart Association, Inc.

---

Effect of Propranolol on Oxygen Binding to Hemoglobin In Vitro and In Vivo

MARSHALL A. LICHTMAN M.D.¹; JULES COHEN M.D.¹; MARION S. MURPHY B.S.¹; ELIZABETH A. KEARNEY B.S.¹; APRIL A. WHITBECK B.S.¹

¹ From the Hematology and Cardiology Units of the Department of Medicine, the Department of Radiation Biology and Biophysics at the University of Rochester School of Medicine and Dentistry, Rochester, New York.

We have shown that propranolol reduces oxygen binding by hemoglobin in intact red cells by increasing the selective permeability of the red cell membrane resulting in an exodus of potassium, chloride, and water. The latter effects result in a new distribution of hydrogen ion between cell and plasma, and thereby a reduction in red cell pH. The reduction in pH can fully explain the change in hemoglobin's affinity for oxygen based on the Bohr effect. Either D- or DL-propranolol can produce the change in red cell pH and oxygen binding by hemoglobin. The drug action on permeability is not prevented by epinephrine, although it is by chlorbutanol. Hence, the membrane action of propranolol does not appear to be related to its activity as a beta-adrenergic receptor blocking agent.

Propranolol produced a marked alteration in red cell shape as well as in hydration (hypovolumic stomatocytes). The two effects were separable since dehydration of the cell by the addition of sucrose to plasma did not result in stomatocytes and chlorbutanol blocked the enhancement of permeability of the red cell membrane by propranolol without preventing the shape change (isovolumic stomatocytes). This suggests that propranolol may have two separate sites of membrane interaction.

Propranolol (10 to 360 mg) administered to human subjects did not affect hemoglobin-oxygen affinity. This is explained by the fact that the concentration in blood after such doses is nearly 4,000 to 100-fold lower than that required to achieve changes in blood in vitro.

Key Words: Erythrocyte • Hemoglobin-oxygen dissociation • Cations • Catecholamines

Submitted on December 4, 1973
Accepted on January 18, 1974

This article has been cited by other articles:

				E. L. Carey JR., D. Robertson, J. N. Wells, and R. M. Robertson Contraction of Isolated Porcine Coronary Arteries is Inhibited by High Concentrations of Propranolol Angiology, June 1, 1995; 46(6): 453 - 460. [Abstract] [PDF]