Lapetina E G, Reep B, Read N G, Moncada S
Thromb Res. 1986 Feb 1;41(3):325-35. doi: 10.1016/0049-3848(86)90243-4.
Prostacyclin (1 ng to 2 micrograms per ml), which effectively inhibits platelet secretion and aggregation, does not affect adhesion of a proportion of platelets (10-38%) to collagen (50-100 micrograms/ml). Adhesion is not detectable by changes of light transmission (as measured in the optical aggregometer) and is not affected by inhibitors of cyclooxygenase and lipoxygenase enzymes such as indomethacin and compound BW 755C. This adhesion is independent of the collagen concentration (50-400 micrograms/ml) and the incubation time (5-20 min). This suggests that adhesion to collagen is related to a specific platelet population. Adhesion in the presence of prostacyclin, indomethacin and BW 755C occurs in parallel with the formation of a limited amount of phosphatidic acid. Under those conditions it is also possible to observe some phosphorylation of a 40,000 dalton protein which is a substrate for protein kinase C activity. Phosphorylation of the 20,000 dalton protein, or myosin light chain, is less evident. Chlorpromazine (25-100 micrograms/ml) inhibited the adhesion of platelets to collagen, but propanolol (0.5-4 microM) was inactive. The adhesion of platelets to collagen in these experiments parallels the formation of a fraction of phosphatidic acid and 40,000 dalton protein phosphorylation, which are independent of the increased levels of platelet cyclic-AMP induced by high concentrations of prostacyclin. It is also independent of the formation of cyclooxygenase or lipoxygenase products.
前列环素（每毫升1纳克至2微克）能有效抑制血小板分泌和聚集，但不影响一部分血小板（10%-38%）与胶原蛋白（每毫升50-100微克）的黏附。通过透光率变化（如在光学聚集仪中测量）无法检测到黏附情况，且其不受环氧化酶和脂氧化酶抑制剂（如吲哚美辛和化合物BW 755C）的影响。这种黏附与胶原蛋白浓度（每毫升50-400微克）和孵育时间（5-20分钟）无关。这表明与胶原蛋白的黏附与特定的血小板群体有关。在前列环素、吲哚美辛和BW 755C存在的情况下，黏附与少量磷脂酸的形成同时发生。在这些条件下，还可以观察到一种40,000道尔顿蛋白质的磷酸化，它是蛋白激酶C活性的底物。20,000道尔顿蛋白质或肌球蛋白轻链的磷酸化不太明显。氯丙嗪（每毫升25-100微克）抑制血小板与胶原蛋白的黏附，但普萘洛尔（0.5-4微摩尔）无此作用。在这些实验中，血小板与胶原蛋白的黏附与一部分磷脂酸的形成以及40,000道尔顿蛋白质的磷酸化同时发生，它们与高浓度前列环素诱导的血小板环磷酸腺苷水平升高无关，也与环氧化酶或脂氧化酶产物的形成无关。
