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《Journal of Xi'an Jiaotong University(Medical Sciences)》 2008-01
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Mechanism of aqueous humor through uveoscleral outflow in rabbits with topical administration of moxonidine

Yang Jiangang1,Cui Lijun1,Quan Yanlong1,Wang Xiaohua1,Zhao Shiping2(1.Department of Ophthalmology;2.Department of Pathology,the Second Affiliated Hospital,Medical School of Xi'an Jiaotong University,Xi'an 710004,China)  
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(P0.05).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 α2 receptor,and then I1 recptor.
【CateGory Index】: R96
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