Yang Jiangang, Sun Naixue, Xiong Quanchen, Yang Rui
Department of Ophthalmology, Second Affiliated Hospital of Medical School, Xi'an Jiaotong University, Xi'an, China.
Curr Eye Res. 2009 Apr;34(4):287-96. doi: 10.1080/02713680902750077.
The purpose of this study is to assess the change of uveoscleral outflow induced by moxonidine and to investigate whether the increase of uveoscleral outflow induced by moxonidine is mediated by alpha1, alpha2, or I1 receptors.
0.05% moxonidine was topically and unilaterally administered in rabbit eyes with or without pretreatment of prazosin, yohimbine, efaroxan, or AGN 192403, as indicated. We injected fluorescein isothiocyanate-bovine serum albumin (FITC-BSA) into the anterior chamber and observed the fluorescence intensity of the uveoscleral outflow. Finally, the volume of uveoscleral outflow was calculated based on the fluorescence intensities captured.
A bilateral increase of fluorescence intensity was observed along the uveoscleral outflow pathway following moxonidine administration, especially in the ciliary body and supraciliochoroidal space. Pretreatment with prazosin further enhanced the bilateral increase of fluorescence intensity at between 2 and 4 hours after moxonidine administration. The response of moxonidine was antagonized by either yohimbine, an alpha2 receptor antagonist, or efaroxan, an I1/alpha2 receptor antagonist. The antagonizing effect of yohimbine was more potent than that of efaroxan. The moxonidne-induced response was not antagonized by AGN 192403, an I1 receptor antagonist. The bilateral volumes of aqueous humor within the uveoscleral pathway increased significantly induced by moxonidine (p < 0.01 versus control). The increased bilateral volumes of uveoscleral outflow were 0.381 +/- 0.073 and 0.376 +/- 0.095 mu l/min, respectively.
These results suggest that topical, unilateral administration of moxonidine causes a bilateral increase of aqueous humor via the uveoscleral outflow pathway. The moxonidine-induced increase of uveoscleral outflow is mediated by alpha2 adrenergic receptors, not by I1 imidazoline receptors.
本研究旨在评估莫索尼定诱导的葡萄膜巩膜流出量的变化，并研究莫索尼定诱导的葡萄膜巩膜流出量增加是否由α1、α2或I1受体介导。
如所示，对兔眼单侧局部给予0.05%莫索尼定，部分兔眼在给药前用哌唑嗪、育亨宾、依酚氯铵或AGN 192403进行预处理。将异硫氰酸荧光素 - 牛血清白蛋白（FITC - BSA）注入前房，并观察葡萄膜巩膜流出途径的荧光强度。最后，根据捕获的荧光强度计算葡萄膜巩膜流出量。
给予莫索尼定后，沿葡萄膜巩膜流出途径观察到荧光强度双侧增加，尤其是在睫状体和睫状体上脉络膜间隙。哌唑嗪预处理在莫索尼定给药后2至4小时进一步增强了荧光强度的双侧增加。莫索尼定的反应被α2受体拮抗剂育亨宾或I1/α2受体拮抗剂依酚氯铵拮抗。育亨宾的拮抗作用比依酚氯铵更强。莫索尼定诱导的反应未被I1受体拮抗剂AGN 192403拮抗。莫索尼定诱导葡萄膜巩膜途径内双侧房水体积显著增加（与对照组相比，p < 0.01）。葡萄膜巩膜流出量双侧增加分别为0.381±0.073和0.376±0.095μl/min。
这些结果表明，局部单侧给予莫索尼定通过葡萄膜巩膜流出途径导致双侧房水增加。莫索尼定诱导的葡萄膜巩膜流出量增加由α2肾上腺素能受体介导，而非I1咪唑啉受体介导。
