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The Peripheral Platelet Count in Response to Adrenergic Alpha‐ and Beta‐1‐Receptor Stimulation
Author(s) -
Fredén Krister,
Lundborg Per,
Vilén Lars,
Kutti Jack
Publication year - 1978
Publication title -
scandinavian journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0036-553X
DOI - 10.1111/j.1600-0609.1978.tb00390.x
Subject(s) - alpha (finance) , stimulation , peripheral , beta (programming language) , adrenergic receptor , platelet , medicine , receptor , endocrinology , computer science , surgery , construct validity , patient satisfaction , programming language
The aim of the present work was to investigate the effect of adrenergic alpha‐ and beta‐1‐receptor stimulation on the peripheral platelet count. The experiments were carried out on 8 healthy male volunteers using radioisotopically labelled platelets. 3 subjects received i.v. infusions of adrenaline (0.09 μg × kg ‐1 × min ‐1 ) before and after the ingestion of 40 mg propranolol. In response to the first infusion there was an instant increase in the venous platelet‐bound radioactivity (PBR) which amounted to 12 % over basal value. This effect of adrenaline seemed to be potentiated by propranolol pretreatment. 5 subjects received i.v. infusions of the highly selective beta‐1‐receptor agonist H 133/22 (prenalterol, Hässle, Sweden). In response to a cumulative dose of 4.75 mg prenalterol a slight but significant (P <0.05) decrease in PBR occurred. It is concluded that alpha‐receptor stimulation causes a depletion of platelets from the exchangeable splenic platelet pool resulting in a concomitant increase in the peripheral platelet count. Beta‐receptor stimulation has an opposite effect on the spleen. The trapping of platelets by the spleen is mediated both via beta‐1‐ and beta‐2‐receptors, but the effect of beta‐2‐receptor stimulation seems to predominate.