Fredén K, Lundborg P, Vilén L, Kutti J
Scand J Haematol. 1978 Nov;21(5):427-32. doi: 10.1111/j.1600-0609.1978.tb00390.x.
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 microgram X kg-1 X 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 less than 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.
本研究的目的是探讨肾上腺素能α受体和β1受体刺激对外周血小板计数的影响。实验在8名健康男性志愿者身上进行,使用放射性同位素标记的血小板。3名受试者在摄入40mg普萘洛尔前后静脉输注肾上腺素(0.09μg·kg-1·min-1)。首次输注后,静脉血小板结合放射性(PBR)立即增加,比基础值高12%。普萘洛尔预处理似乎增强了肾上腺素的这种作用。5名受试者静脉输注高选择性β1受体激动剂H 133/22(普瑞特罗,瑞典哈塞尔公司)。累积剂量为4.75mg普瑞特罗时,PBR出现轻微但显著(P<0.05)下降。结论是,α受体刺激导致可交换脾血小板池中的血小板消耗,从而使外周血小板计数相应增加。β受体刺激对脾脏有相反的作用。脾脏对血小板的捕获通过β1受体和β2受体介导,但β2受体刺激的作用似乎占主导。