Yanaura S, Hosokawa T, Goto K, Misawa M
J Pharmacobiodyn. 1981 Sep;4(9):685-90. doi: 10.1248/bpb1978.4.685.
Participation of histamine H1- and H2-receptors in the bronchial musculature and vasculature of the dog was investigated by using the method for evaluating airway responses. A peristaltic pump and a Starling pneumatic resistance were used for a constant pressure perfusion. Dogs given 0.1 - 10 micrograms histamine by a close intraarterial injection showed increases in ventilation overflow (bronchoconstriction) and in blood flow (bronchial vasodilatation) in a dose-dependent manner. The bronchoconstriction produced by histamine was antagonized strongly by chlorpheniramine, a H1-receptor antagonist, but not modified by cimetidine, a H2-receptor antagonist. The bronchial vasodilation produced by histamine was antagonized by both chlorpheniramine and cimetidine. These results suggest that histamine evokes bronchoconstriction through H1-receptors and bronchial vasodilatation through H1- and H2-receptors.
通过使用评估气道反应的方法,研究了组胺H1和H2受体在犬支气管肌肉组织和血管系统中的参与情况。使用蠕动泵和史塔林气动阻力进行恒压灌注。通过动脉内近距离注射给予犬0.1 - 10微克组胺后,通气溢出(支气管收缩)和血流量(支气管血管舒张)呈剂量依赖性增加。组胺产生的支气管收缩被H1受体拮抗剂氯苯那敏强烈拮抗,但未被H2受体拮抗剂西咪替丁改变。组胺产生的支气管血管舒张被氯苯那敏和西咪替丁均拮抗。这些结果表明,组胺通过H1受体引起支气管收缩,并通过H1和H2受体引起支气管血管舒张。