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作 者:杨建刚[1] 崔丽珺[1] 权彦龙[1] 王肖华[1] 赵世平[2]
机构地区:[1]西安交通大学医学院第二附属医院眼科,陕西西安710004 [2]西安交通大学医学院第二附属医院病理科,陕西西安710004
出 处:《西安交通大学学报(医学版)》2008年第1期51-53,56,共4页Journal of Xi’an Jiaotong University(Medical Sciences)
摘 要:目的观察I1受体激动剂莫索尼定滴眼对葡萄膜巩膜途径各部位荧光强度的变化,研究莫索尼定对葡萄膜巩膜途径房水外流的作用机制。方法莫索尼定单侧滴眼,示踪剂FITC-BSA双眼前房注入,2-10 h不同时点冰冻切片,荧光显微镜下观察葡萄膜巩膜途径各部位的荧光强度;prazosin(α1受体拮抗剂)、yohimbine(α2受体拮抗剂)和efaroxan(I1受体拮抗剂)前处理30 min,莫索尼定滴眼,观察葡萄膜巩膜途径荧光变化。结果莫索尼定滴眼荧光显微镜观察,双侧葡萄膜巩膜途径荧光强度明显增强,以睫状体和脉络膜上腔较强。prazosin前处理组各部位与莫索尼定比较荧光强度无显著性差异,yohimbine和efaroxan前处理组双侧荧光强度各部位均较莫索尼定组减弱,差异有统计学意义(P<0.01),yohimbine较efaroxan前处理组荧光更弱。结论莫索尼定可增加房水经葡萄膜巩膜途径外流,与prazosin产生协同作用,yohimbine和efaroxan均可抑制双侧葡萄膜巩膜途径房水外流的增加,yohimbine的抑制作用更显著,说明葡萄膜巩膜途径房水外流主要由α2受体介导,I1受体也产生作用。Objective To investigate the changes of uveoscleral pathway by an I1 receptor agonist, moxonidine, and with pretreatment of antagonists topical administration, and to study the mechanism that moxonidine improves uveoscleral outflow. Methods Moxonidine was administered unilaterally and topically to rabbits and with pretreatment of the antagonists, namely, prazosin, yohimbine and efaroxan. FITC-BSA, a tracer agent, was injected into the anterior chamber after moxonidine treatment or with pretreatment of the antagonists. Frozen sections were undertaken at different time points between 2 to 10 h. Fluorescence intensity was observed in the sites of uveoscleral pathway in the sections by fluorescence microscopy. Results Bilateral fluorescence intensity treated with moxonidine was more intense than that with placebo, and the most intense regions of fluorescence were ciliary body and superchoroidal space. Fluorescence intensity by prazosin pretreatment was not significantly different compared to that by moxonidine, while yohimbine and efaroxan pretreatment decreased the intensity compared with moxonidine (P 〈 0. 05). Yohimbine was more significant effectively than efaroxan. Conclusion Topical administration of moxonidine increased uveoscleral outflow. Prazosin pretreatment produced the synergy with moxonidine, whereas yohimbine and efaroxan inhibited the effect of moxonidine. The inhibition by yohimbine was more significant in uveoscleral pathway. It indicates that the mechanism of moxonidine, in uveoscleral pathway is firstly moderated by az receptor, and then I1 recptor.
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