Compton M R, Seale J P, Shaw J
Arch Int Pharmacodyn Ther. 1985 Jul;276(1):112-9.
The anaphylactic mediators, histamine and leukotrienes, stimulate arachidonic acid (AA) metabolism in the guinea-pig lungs, leading to the synthesis and release of thromboxane A2 (TxA2) and other cyclo-oxygenase products. Since TxA2 is a potent bronchoconstrictor, it is possible that the activation of AA metabolism by histamine may contribute to the pulmonary manifestations of anaphylaxis. In the present experiments, histamine-induced release of TxA2 was inhibited by mepyramine (10(-8)-10(-6) M) but not by cimetidine (5 X 10(-5) M) indicating that the release was mediated by H1-receptors. The beta-adrenoceptor agonists, fenoterol (10(-6) M) and isoprenaline (10(-6) M) inhibited the histamine-induced release of TxA2. This effect was partially reversed by propranolol. These results suggest that if histamine-induced TxA2 release is involved in guinea-pig pulmonary anaphylaxis then inhibition of this release may be a factor in the anti-anaphylactic effect of beta-adrenoceptor agonists.
过敏介质组胺和白三烯可刺激豚鼠肺组织中的花生四烯酸（AA）代谢，导致血栓素A2（TxA2）及其他环氧化酶产物的合成与释放。由于TxA2是一种强效支气管收缩剂，组胺激活AA代谢可能是过敏反应肺部表现的原因之一。在本实验中，美吡拉敏（10(-8)-10(-6)M）可抑制组胺诱导的TxA2释放，而西咪替丁（5×10(-5)M）则无此作用，表明该释放是由H1受体介导的。β-肾上腺素能受体激动剂非诺特罗（10(-6)M）和异丙肾上腺素（10(-6)M）可抑制组胺诱导的TxA2释放。普萘洛尔可部分逆转此作用。这些结果提示，如果组胺诱导的TxA2释放参与豚鼠肺部过敏反应，那么抑制该释放可能是β-肾上腺素能受体激动剂抗过敏作用的一个因素。
