Cioffi G A, Sullivan P
Devers Eye Institute, Portland, Oregon, USA.
Eur J Ophthalmol. 1999 Jan-Mar;9 Suppl 1:S34-6. doi: 10.1177/112067219900901S12.
To develop an in vivo model of chronic optic nerve ischemia to study the role of vascular insufficiency in the development of glaucomatous optic neuropathy.
We surgically implanted osmotically-driven mini-pumps that allowed the continuous micro-application of 0.2 micrograms/day of endothelin-1 (ET-1) into the retrobulbar optic nerve of rabbits and rhesus monkeys. ET-1 was delivered for 2 to 6 months, following which histological studies were performed.
Both rabbits and primates experienced a 35% to 38% decrease in optic nerve blood flow with corresponding focal narrowing of the vessels supplying the optic nerve. In the rabbit model, optic disc excavation and histologic tissue loss in the anterior optic nerve resulted from the induced ischemia.
Chronic ischemia of the primate anterior optic nerve induced with endothelin-1 infusion resulted in diffuse loss of axons without a change in the intraocular pressure.
建立慢性视神经缺血的体内模型,以研究血管功能不全在青光眼性视神经病变发生发展中的作用。
我们通过手术将渗透驱动微型泵植入兔和恒河猴的球后视神经,该微型泵可每天持续微量注入0.2微克内皮素-1(ET-1)。ET-1持续给药2至6个月,之后进行组织学研究。
兔和灵长类动物的视神经血流量均减少了35%至38%,同时供应视神经的血管出现相应的局灶性狭窄。在兔模型中,诱导的缺血导致视盘凹陷和视神经前部的组织学组织丢失。
通过注入内皮素-1诱导的灵长类动物视神经前部慢性缺血导致轴突弥漫性丢失,而眼压无变化。