Umemoto M, Tanaka H, Miichi H, Hayashi S
Research and Development Division, Rohto Pharmaceutical Co., Ltd., Osaka, Japan.
Ophthalmic Res. 1987;19(4):200-4. doi: 10.1159/000265494.
The role of histamine H1- and H2-receptors in mediating the response produced by histamine was investigated on rat ocular surface. Histamine caused a dose-dependent increase in microvascular permeability on this surface. Response to histamine was significantly inhibited by pretreatment with chlorpheniramine (an H1-antagonist) but was unchanged by cimetidine (an H2-antagonist). No additive effect was shown when chlorpheniramine and cimetidine were used in combination. Moreover, dimaprit, a selective histamine H2-receptor agonist, failed to elicit a dose-dependent vasopermeability response. Chlorpheniramine significantly reduced increase in microvascular permeability associated with immediate hypersensitivity, although cimetidine did not. The addition of cimetidine to chlorpheniramine did not lead to greater reduction than that achieved with chlorpheniramine alone. We conclude that the microvascular permeability response to histamine is predominantly mediated by H1-receptors on rat ocular surface.
研究了组胺H1和H2受体在介导大鼠眼表组胺产生的反应中的作用。组胺使该眼表微血管通透性呈剂量依赖性增加。用氯苯那敏（一种H1拮抗剂）预处理可显著抑制对组胺的反应，但西咪替丁（一种H2拮抗剂）对其无影响。氯苯那敏和西咪替丁联合使用未显示出相加作用。此外，选择性组胺H2受体激动剂二甲双胍未能引发剂量依赖性的血管通透性反应。氯苯那敏显著降低了与速发型超敏反应相关的微血管通透性增加，尽管西咪替丁没有。在氯苯那敏中加入西咪替丁并没有比单独使用氯苯那敏产生更大程度的降低。我们得出结论，大鼠眼表对组胺的微血管通透性反应主要由H1受体介导。
