Siess W, Lorenz R, Roth P, Weber P C
Agents Actions. 1983 Feb;13(1):29-34. doi: 10.1007/BF01994278.
In vitro and ex vivo effects of propranolol on platelet aggregation, formation of thromboxane B2 (TXB2) and platelet sensitivity to prostacyclin were studied in healthy men. Propranolol, added in vitro to platelet rich plasma (PRP) inhibited platelet aggregation and TXB2 formation induced by ADP, 1-epinephrine, collagen and arachidonic acid. Concentrations of 20-100 microM propranolol were effective when ADP, 1-epinephrine and collagen were used as stimuli. Higher concentrations (250-500 microM) were needed to inhibit aggregation induced by arachidonic acid. Oral administration of propranolol either as a single dose (120 mg) or for one week (3 x 40 mg/day) did, however, not affect platelet aggregation, thromboxane formation and platelet sensitivity to prostacyclin. In addition, withdrawal of propranolol was without effect on these parameters. Although propranolol has potent effects on platelet function in vitro, it seems that the blood levels achievable by oral administration of propranolol are too low to affect platelet aggregation and TXB2 formation.
在健康男性中研究了普萘洛尔对血小板聚集、血栓素B2(TXB2)形成及血小板对前列环素敏感性的体外和离体效应。体外向富血小板血浆(PRP)中添加普萘洛尔可抑制由ADP、肾上腺素、胶原和花生四烯酸诱导的血小板聚集及TXB2形成。当以ADP、肾上腺素和胶原作为刺激物时,20 - 100微摩尔浓度的普萘洛尔有效。抑制花生四烯酸诱导的聚集则需要更高浓度(250 - 500微摩尔)。然而,口服单剂量(120毫克)或连续一周(每日3次,每次40毫克)的普萘洛尔均不影响血小板聚集、血栓素形成及血小板对前列环素的敏感性。此外,停用普萘洛尔对这些参数也无影响。虽然普萘洛尔在体外对血小板功能有显著作用,但口服普萘洛尔所能达到的血药浓度似乎过低,不足以影响血小板聚集和TXB2形成。