Thiemermann C, Lidbury P S, Thomas G R, Vane J R
William Harvey Research Institute, St. Bartholomew's Hospital Medical College, London, England.
J Cardiovasc Pharmacol. 1989;13 Suppl 5:S138-41; discussion S142.
The effects of porcine endothelin (endothelin-1, ET-1; 1 nmol/kg i.a.) on ex vivo platelet aggregation and platelet cAMP/cGMP levels were investigated in the anesthetized rabbit. ET-1 inhibited ADP-induced platelet aggregation by 83 +/- 9% within 5 min (p less than 0.01). This ET-1-induced inhibition of platelet aggregation lasted for 30 min and was associated with a significant (five- to sixfold) increase in platelet cAMP. However, platelet cGMP levels were unaffected. Indomethacin (5 mg/kg i.v., 20 min prior to ET-1) abolished the ET-1-induced inhibition of ex vivo platelet aggregation as well as the corresponding augmentation of platelet cAMP. Thus, ET-1 inhibits platelet function in vivo due to the release into the circulation of antiplatelet cyclo-oxygenase products, such as prostacyclin (or PGD2).
在麻醉兔中研究了猪内皮素（内皮素-1，ET-1；1 nmol/kg腹腔注射）对体外血小板聚集及血小板cAMP/cGMP水平的影响。ET-1在5分钟内将ADP诱导的血小板聚集抑制了83±9%（p<0.01）。ET-1诱导的这种血小板聚集抑制持续30分钟，并与血小板cAMP显著（五至六倍）增加相关。然而，血小板cGMP水平未受影响。吲哚美辛（5 mg/kg静脉注射，在ET-1注射前20分钟）消除了ET-1诱导的体外血小板聚集抑制以及相应的血小板cAMP增加。因此，ET-1在体内抑制血小板功能是由于抗血小板环氧化酶产物如前列环素（或PGD2）释放到循环中。
