Greer I A, Walker J J, Calder A A, Forbes C D
Thromb Res. 1985 Dec 1;40(5):631-43. doi: 10.1016/0049-3848(85)90301-9.
It has recently become possible to study platelet aggregation in whole blood which may more closely resemble the in-vivo situation as the platelets are left in their natural milieu with red and white cells present which themselves can influence aggregation. The effects of 4 adrenoceptor antagonists on platelet aggregation in whole blood were studied in-vitro using the Clay-Adams Ultra Flo 100 whole blood platelet counter. Labetalol, pindolol and propranolol inhibited aggregation to 0.5 microgram/ml collagen in a dose dependent manner, and were synergistic with prostacyclin in inhibiting collagen induced aggregation. These 3 drugs also promoted reversal of aggregation induced by 10 microM ADP, but only inhibited 0.5 mM arachidonic acid induced aggregation at high drug concentrations. Atenolol had no effect on either collagen, ADP or arachidonic acid induced aggregation. The anti-platelet effect of these drugs may be of value in the treatment of vascular disease.
最近,已经能够在全血中研究血小板聚集,由于血小板处于含有红细胞和白细胞的自然环境中,而红细胞和白细胞本身会影响聚集,因此全血中的血小板聚集可能更接近体内情况。使用Clay-Adams Ultra Flo 100全血血小板计数器在体外研究了4种肾上腺素能受体拮抗剂对全血中血小板聚集的影响。拉贝洛尔、吲哚洛尔和普萘洛尔以剂量依赖的方式抑制对0.5微克/毫升胶原蛋白的聚集,并且在抑制胶原蛋白诱导的聚集方面与前列环素具有协同作用。这3种药物还促进了由10微摩尔/升二磷酸腺苷诱导的聚集的逆转,但仅在高药物浓度下抑制0.5毫摩尔/升花生四烯酸诱导的聚集。阿替洛尔对胶原蛋白、二磷酸腺苷或花生四烯酸诱导的聚集均无影响。这些药物的抗血小板作用可能在血管疾病的治疗中有价值。