Vargaftig B B, Lefort J
Prostaglandins. 1979 Oct;18(4):519-28. doi: 10.1016/0090-6980(79)90020-0.
The antagonism by prostacyclin (PG12) and prostaglandin E1 (PGE1) of bronchoconstriction induced by serotonin (5HT), collagen, arachidonic acid (AA) and anaphylaxis, as well as of thrombocytopenia was studied in the guinea-pig. Under conditions where PGE1 prevented bronchoconstriction by 5HT, by collagen or by AA better than the accompanying thrombocytopenia, PG12 was a selective antagonist of bronchoconstriction due to collagen, but failed to interfere with that due to 5HT or to AA. Collagen-induced bronchoconstriction in the guinea-pig is platelet-dependent. PG12 blocks bronchoconstriction by collagen, because it prevents the platelet activation, and fails to interfere with bronchoconstriction by AA, even though it reduces the accompanying thrombocytopenia, because the role of platelets is negligible. PGE1 and PG12 failed to interfere with thrombocytopenia or with bronchoconstriction of anaphylactic shock, and were inactive even when the acute bronchial effect was suppressed by anti-histamine treatment. Anaphylactic thrombocytopenia is beyond the control of agents which stimulate the cyclic AMP system, and involves specific mechanism which are not stimulated in platelet-rich plasma.
在豚鼠中研究了前列环素(PGI₂)和前列腺素E₁(PGE₁)对5-羟色胺(5-HT)、胶原、花生四烯酸(AA)和过敏反应所诱导的支气管收缩以及血小板减少的拮抗作用。在PGE₁比伴随的血小板减少更能有效预防5-HT、胶原或AA所诱导的支气管收缩的条件下,PGI₂是胶原所致支气管收缩的选择性拮抗剂,但对5-HT或AA所致的支气管收缩无干扰作用。豚鼠中胶原诱导的支气管收缩依赖于血小板。PGI₂通过阻止血小板活化来阻断胶原诱导的支气管收缩,尽管它能减轻伴随的血小板减少,但对AA诱导的支气管收缩无干扰作用,因为血小板在其中的作用可忽略不计。PGE₁和PGI₂对血小板减少或过敏性休克的支气管收缩均无干扰作用,即使在用抗组胺治疗抑制急性支气管效应时也无活性。过敏性血小板减少不受刺激环磷酸腺苷系统的药物控制,且涉及在富含血小板血浆中未被刺激的特定机制。