Togias A, Proud D, Kagey-Sobotka A, Norman P, Lichtenstein L, Naclerio R
J Allergy Clin Immunol. 1987 Apr;79(4):599-604. doi: 10.1016/s0091-6749(87)80155-0.
We have previously demonstrated that azatadine, a tricyclic antihistamine, known also to inhibit mediator release from mast cells and basophils in vitro, inhibits the early release of histamine and other mediators after nasal challenge with antigen. In this article, we studied the effect of azatadine on preventing the release of histamine after nasal challenge with cold, dry air (CDA) and its effect on antagonizing nasal challenge with histamine. With histamine challenge, azatadine inhibited symptoms (sneezing, nasal congestion, and rhinorrhea) and the increase in the level of albumin in nasal secretions (p less than 0.01 all). With challenge with CDA, the drug had no effect on either symptoms or histamine and N-tosyl-L-arginine methyl ester-esterase release. Although the patterns of mediator release after CDA and after the early reaction to antigen are similar, the pharmacologic control differs, suggesting different mechanisms of induction of histamine release from mast cells.
我们之前已经证明，氮卓斯汀，一种三环类抗组胺药，已知在体外也能抑制肥大细胞和嗜碱性粒细胞释放介质，它能抑制抗原鼻腔激发后组胺和其他介质的早期释放。在本文中，我们研究了氮卓斯汀对预防冷干空气（CDA）鼻腔激发后组胺释放的作用及其对组胺鼻腔激发的拮抗作用。对于组胺激发，氮卓斯汀可抑制症状（打喷嚏、鼻塞和流涕）以及鼻分泌物中白蛋白水平的升高（均P<0.01）。对于CDA激发，该药物对症状或组胺及N-对甲苯磺酰-L-精氨酸甲酯酯酶的释放均无作用。尽管CDA激发后和对抗原早期反应后介质释放模式相似，但药物控制不同，提示肥大细胞组胺释放的诱导机制不同。
