Nonaxoplasmic transfer of indocyanine green into the optic nerve after intravitreal application.
Nonaxoplasmic transfer of indocyanine green into the optic nerve after intravitreal application.
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DOI：
10.1097/00006982-200506000-00031
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发表时间：
2005-06
期刊：
影响因子：
--
通讯作者：
M. Pâques
中科院分区：
文献类型：
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作者：
M. Pâques
我带着极大的兴趣阅读了最近的文章，作者是J.E.K.等人1，关于玻璃体内吲哚菁绿色（ICG）的眼后迁移机制。他们报告ICG的迁移仅限于视神经的前部，不会扩散到视交叉;因此，可能是由于非轴浆转运。后者可能是由于轴突周围脂质（如髓鞘）的浸润以及玻璃体液穿过视神经的转移，2，3，ICG不会扩散到视交叉后方。正如Zakekikiovan等人所指出的，他们的数据似乎与我的小组以前的研究有些矛盾。[4]事实上，使用类似的方法，我们发现ICG快速而一致地向上迁移到上级丘。此外，运输ICG到离散轴突囊泡被证实由红外光学显微镜。因此，在我们看来，除了非特异性轴浆外扩散外，ICG被主动转运到轴突中似乎是毫无疑问的。不幸的是，Eschekikienet等人没有讨论这些差异的可能来源。我要强调以下几点。首先，气体玻璃体切除术可能引起眼内压升高，随后损伤视网膜神经节细胞和轴突运输改变。因此，报告其气体玻璃体切除眼的眼内压和组织学数据可能是有意义的。在没有轴突运输阻滞的手术眼中使用参考示踪剂可能有助于确定是否确实存在顺行轴突运输的持续性。第二，只有两只眼睛接受了ICG注射到玻璃体中，而没有玻璃体切除术，这些动物在第1天进行了检查，但没有在以后。根据我们的数据，在第1天，ICG只会向后迁移几毫米。Kriekikiovan et al未指出是否在随后的时间点检查了非玻璃体切除ICG注射动物。
I read with great interest the recent article by Çekiç et al1 about the mechanisms involved in retroocular migration of intravitreal indocyanine green (ICG). They reported that migration of ICG is limited to the anterior portion of the optic nerve and does not spread to the chiasma; therefore, it is likely to be due to nonaxoplasmic transport. The latter is probably due to impregnation of periaxonal lipids, such as myelin, and to vitreal fluid shift across the optic nerve, 2, 3 and ICG does not diffuse posterior to the chiasma. As indicated by Çekiç et al, their data appear somewhat contradictory to those of a previous study by my group. 4 Indeed, using similar methods, we found that ICG rapidly and consistently migrated up to the superior colliculus. In addition, the transport of ICG into discrete axonal vesicles was confirmed by infrared light microscopy. Therefore, in our opinion, there appears to be little doubt that ICG is actively transported into axons, in addition to nonspecific extraaxoplasmic diffusion. Unfortunately, Çekiç et al did not discuss the possible sources of these discrepancies. I would like to underline the following points. First, the gas vitrectomy procedure is likely to provoke an increase in intraocular pressure and subsequently damage to retinal ganglion cells and alteration of axonal transport. Reporting intraocular pressure and histologic data for their gas-vitrectomized eyes could therefore be of interest. Using a reference tracer in operated eyes without axonal transport blockade could be useful to determine if there was indeed persistence of anterograde axonal transport. Second, only two eyes underwent ICG injection into the vitreous without vitrectomy, and these animals were examined on day 1 but not later on. According to our data, on day 1, ICG would have migrated only a few millimeters posteriorly. Çekiç et al did not indicate if nonvitrectomized ICG-injected animals were examined at later time points.