Fortune Brad, Cull Grant, Wang Lin, Van Buskirk E Michael, Cioffi George A
Discoveries in Sight Research Laboratories, Devers Eye Institute, Portland, OR 97232, USA.
Doc Ophthalmol. 2002 Sep;105(2):151-78. doi: 10.1023/a:1020548919355.
While elevated intraocular pressure (IOP) undoubtedly plays a crucial role in many glaucoma patients, vascular dysregulation and chronic regional ischemia are also thought to contribute to the pathophysiology of glaucoma. In an effort to critically evaluate hypotheses involving vascular abnormalities in glaucoma, Cioffi, Van Buskirk and co-workers have developed a model of optic neuropathy based on chronic regional ischemia. The multifocal electroretinogram (MERG) has previously been used to assess function in non-human primates with experimental glaucoma induced by high-IOP. In this study, the MERG was used to monitor function in macaque monkeys with experimental glaucoma induced by chronic anterior optic nerve ischemia. Initial recordings from experimental eyes, which were later documented histologically to have moderate axon loss, revealed little difference from recordings of control eyes. This suggested that many of the signal components in the macaque MERG, which are known (from other studies) to be eliminated by intravitreal injections of NMDA/TTX or by high-IOP experimental glaucoma, may also be affected by the choice of anesthetic agents and MERG recording parameters. Subsequent experiments were performed to specifically evaluate the effects of bipolar versus monopolar signal derivation, anesthetic agents, MERG stimulus design and spatial scale. The results demonstrate that successful measurement of inner retinal and optic nerve head MERG components, especially those which have been shown by other investigators to originate with ganglion cell spiking activity, will depend critically upon the choice of anesthetic agents and recording parameters. One of the most important parameters seems to be use of a monopolar signal derivation, with the contralateral cornea serving as the reference position.
虽然眼内压(IOP)升高在许多青光眼患者中无疑起着关键作用,但血管调节异常和慢性局部缺血也被认为与青光眼的病理生理学有关。为了严格评估涉及青光眼血管异常的假说,乔菲、范·布斯柯克及其同事基于慢性局部缺血开发了一种视神经病变模型。多焦视网膜电图(MERG)此前已用于评估高眼压诱导的实验性青光眼的非人灵长类动物的功能。在本研究中,MERG用于监测慢性视神经前部缺血诱导的实验性青光眼猕猴的功能。实验眼的初始记录(后来经组织学证实有中度轴突损失)与对照眼的记录显示差异不大。这表明猕猴MERG中的许多信号成分(从其他研究中已知)可通过玻璃体内注射NMDA/TTX或高眼压实验性青光眼消除,也可能受麻醉剂选择和MERG记录参数的影响。随后进行了实验,以具体评估双极与单极信号导出、麻醉剂、MERG刺激设计和空间尺度的影响。结果表明,成功测量视网膜内层和视神经乳头MERG成分,尤其是其他研究者已证明起源于神经节细胞放电活动的那些成分,将严重依赖于麻醉剂的选择和记录参数。最重要的参数之一似乎是使用单极信号导出,对侧角膜作为参考位置。