Protective effect of dextromethorphan on the ischemic retinal damage in rabbit]

To investigate the effect of dextromethorphan (DEX), N-methyl-D-aspartate (NMDA) receptor antagonist, on the retinal ischemia, 0.4%DEX hydrobromide was intravenously given to rabbits before, during and after retinal ischemia. Retinal function was monitored by electroretinogram (ERG). Retinal ischemia was induced by increasing intraocular pressure to 130 mmHg for 90 or 120 min. Amplitudes of ERG.b-waves recorded after the 90 min ischemia recovered to 72.5 +/- 9.0% in the DEX group and 38.5 +/- 8.5% in the control group which was given normal saline. The maximal recovery rates of b-wave amplitudes after the 120 min ischemia were 44.0 +/- 7.9% in the DEX group and 21.0 +/- 1.3% in the control group. The recovery rates of the b-wave amplitudes in DEX group were significantly higher than in the control group (p less than 0.01). It was found that the effective dose of DEX was 0.1-0.4%.     

中药黄斑方剂对大鼠光损伤后视网膜功能的防护作用

目的探讨中药黄斑方剂对大鼠光照后视网膜功能的影响。方法建立SD大鼠光损伤模型。14只大鼠随机分为治疗组和对照组。治疗组光照前2d给予黄斑方剂灌胃治疗,对照组给予相同容量的蒸馏水。视网膜电图(ERG)检钡4光照前后不同时间点暗视ERGb波振幅的变化。结果光照前SD大鼠均可引出典型的F-ERG波形,光照后3、7和14d,ERGb波振幅分别为光照前的33%、30%和32%。而治疗组ERGb波振幅降低幅度较对照组明显降低,分别为光照前的61%、59%和64%,差异具有统计学意义。结论持续光照可导致ERGb波振幅明显下降,中药黄斑方剂对视网膜功能具有部分防护作用。     

实验性急性高眼压对兔视网膜电图的影响

目的：检测家兔实验性急性高眼压不同压力状态下视网膜电图的变化。方法：采用视电生理检测仪测定家兔实验前,30mmHg(1mmHg=0.133kPa),60mmHg,90mmHg和120mmHg前房高压灌注45min及恢复正常眼压4h的视网膜电图（Flash Electroretinogram FERG)和振荡电位（Oscillatory Potentials,OPs)。结果：对照组和30mmHg组视电生理检测在实验前后无差异。60mmHg组在高压持续45min后,b波和OPs波振幅下降,4h后恢复正常。90mmHg和120mmHg组在高压45min后,FERG波形消失。4h后有不同程度恢复。结论：随着实验性高眼压压力的升高,家兔视网膜功能损伤加重,恢复能力减弱。     

Functional characterization of retina and optic nerve after acute ocular ischemia in rats

PURPOSE: To functionally characterize the status of the rat retina and optic nerve after acute elevation of intraocular pressure (IOP) and to determine the dynamics of the pathologic changes in the ischemic retina and optic nerve. METHODS: Retinal ischemia was induced in rats by acutely increasing the IOP (110 mm Hg/60 minutes). Direct and indirect pupil light reflexes (PLRs) were recorded from the noninjured eye, and electroretinograms (flash and flicker ERG) were recorded from the injured and control eyes before and after surgery. Amplitudes and latencies were calculated for each recording session. RESULTS: Preoperative PLR(ratio)s (indirect/direct PLR) were 76.7 +/- 2.6 (mean +/- SEM). Twenty-four hours after surgery the PLR(ratio) was 15.2 +/- 12.8, 10 days after surgery, 11.6 +/- 9.8; 20 days after surgery, 26.5 +/- 8.0; and 28 days after surgery, 33.27 +/- 9.3. However, at day 35, the PLR had significantly recovered (41.1 +/- 7.3) when compared with the 24-hour postoperative ratios (P < 0.01, repeated-measures ANOVA). Forty-two days after surgery, the PLR(ratio) started to decrease once again in the injured eyes (28.7 +/- 5.9). Electroretinographic amplitudes (full-field flash ERG) followed a similar pattern. Cone responses (flicker ERG) were measured 42 days after surgery and revealed defects in injured eyes (control eyes: 46.6 +/- 2.9 microV, injured eyes: 3.4 +/- 1.7 microV). Histologic analysis revealed ischemic damage to all retinal layers, with the primary defects localized to the central retina. CONCLUSIONS: Acute ocular ischemia causes a significant decrease in retinal function, as measured by PLR and ERG, although over time the rat retina and optic nerve show partial regain of function.     

Neuroprotective Effect of the Novel Na+/Ca2+ Channel Blocker NS-7 on Rat Retinal Ganglion Cells

Purpose

To investigate whether NS-7, 4-(4-fluorophenyl)-2-methyl-6-(5-piperidinopentyloxy) pyrimidine hydrochloride, a novel Na⁺/Ca²⁺ channel blocker, can protect the rat retina subjected to ischemia–reperfusion insult.

Methods

To evaluate the protective effect of NS-7 against retinal damage, the drug was administered before and after ischemia–reperfusion. Damage to the retina was assessed by measuring the thickness of the inner plexiform layer (IPL) and the outer nuclear layer (ONL) of each eye. In a subsequent experiment, electroretinographic (ERG) evaluation was also used.

Results

In histopathologic evaluation, ischemia–reperfusion injury caused a significant reduction of IPL thickness (measured as the IPL/ONL ratio). In the NS-7-treated group, retinal damage was partially prevented by a concentration of 0.25?mg/kg per day. In the ERG evaluation, ischemia–reperfusion injury caused a reduction of A- and B-wave amplitudes. NS-7 treatment significantly prevented the reduction of the B wave at a concentration of 0.1 or 0.3?mg/kg, while the reduction of the A wave was not significantly affected.

Conclusions

NS-7 has neuroprotective effects against retinal damage resulting from subjection to ischemia. In addition, NS-7 can be used as an agent for treating acute ischemic retinopathy, including diseases associated with very high intraocular pressure, such as acute angle-closure glaucoma. Jpn J Ophthalmol 2005;49:371–376 © Japanese Ophthalmological Society 2005     

Impaired electroretinogram (ERG) response in apolipoprotein E-deficient mice

PURPOSE: We investigated the effects of 35 weeks of a cholesterol diet in apolipoprotein E (apoE)-deficient mice on their ERG response. METHODS: C57BL/6J and apoE-deficient mice were fed regular mouse chow (C57-R and ApoE-R, respectively) or a cholesterol-containing diet (C57-C and ApoE-C, respectively). Retinal function was assessed by dark-adapted electroretinography (ERG). Retina tissue was also analyzed by immunohistochemical staining and nucleic acid array expression analysis performed by gene array technology. RESULTS: ApoE-C mice had diminished a- and b-wave amplitudes (60.7% +/- 8.4% (p < 0.005) and 44.8% +/- 10% (p < 0.005) of control values, respectively). Gene expression profiling revealed upregulation of several pro-apoptotic genes. Furthermore, immunohistochemistry showed increased Bax immunoreactivity. CONCLUSIONS: In the hypercholesterolemic mice, we demonstrated a loss of ERG response and induction of apoptotic activity at the gene and protein levels. Our current and previous findings suggest that cholesterol metabolism plays an important role in retinal function.     

Neuroprotective effects of eliprodil in retinal excitotoxicity and ischemia

PURPOSE: To evaluate whether eliprodil (SL82.0715), a NR2B-selective N-methyl-D-aspartate (NMDA) antagonist, is protective of retina subjected to an excitotoxic or ischemic insult. METHODS: To evaluate protection against retinal excitotoxicity, eliprodil was administered intraperitoneally before and after the injection of NMDA (5 microl, 20 nmol) into the vitreous of rats. Integrity of the retina was assessed by counting cells in the retinal ganglion cell layer (GCL) and measuring choline acetyltransferase (ChAT) activity. In a subsequent experiment, total retinal ischemia, as measured by a cessation of electroretinographic (ERG) activity, was induced in anesthetized rabbits by elevating intraocular pressure above systolic blood pressure for 65 minutes. After ischemia, recovery of ERG activity was assessed at 24 and 48 hours in animals treated with vehicle or eliprodil (1.0-10.0 mg/kg). RESULTS: Intravitreal NMDA injection resulted in a dose-related decrease in cells of the GCL and in ChAT activity. Eliprodil administered intraperitoneally at 10 mg/kg completely prevented the loss of ChAT and the loss of cells in the GCL. Twenty-four hours after retinal ischemia, A and B waves of vehicle-treated animals were suppressed by 60% to 70%. Eliprodil administered intraperitoneally at 10 mg/kg ameliorated the A- and B-wave depression throughout the 48-hour experiment. CONCLUSIONS: Eliprodil is neuroprotective of retinae subjected to either an excitotoxic or ischemic challenge and may be useful for treating a variety of retinal and optic nerve head disorders.     

Delayed treatment with dextromethorphan can reduce ischemic retinal damage in rabbit]

Previous studies have suggested that prophylactic treatment by dextromethorphan (DEX), N-methyl-D-aspartate (NMDA) receptor antagonist can protect the retina against ischemia. To investigate the effect of DEX on the proceeding ischemic retina, 0.1% DEX hydrobromide was intravenously administered in rabbits immediately (group A), 1 hour (group B) or 2 hours (group C) after the release from ischemia induced by increasing intraocular pressure to 130 mmHg for 90 min. Normal saline was infused immediately after the release from ischemia as control rabbits. Retinal function was monitored by recording electroretinogram (ERG). Twenty four hours after the release of ischemia, the recovery rates of ERG.b-wave amplitudes in groups A, B and C were 61.3 +/- 3.3, 52.2 +/- 9.0 and 43.6 +/- 8.4% of the preischemic amplitude, respectively. The recovery rate of the group A was higher than that of the control (41.9 +/- 10.6%), while no significant differences were seen between groups B or C and the control. The results suggest that DEX can protect the retina if it is administered immediately after the release of ischemia.     

Possible implications of acid-sensing ion channels in ischemia-induced retinal injury in rats

Background

Retinal ischemia in eyes with diabetic retinopathy and retinal vein occlusion leads to local tissue acidosis. Acid-sensing ion channels (ASICs) are expressed in photoreceptors and other neurons in the retina, and may play a role in acid-induced cell injury. The purpose of this study was to investigate the neuroprotective effects of amiloride, an ASIC blocker, on induced retinal ischemia in rats.

Methods

Transient retinal ischemia was induced in male Long–Evans rats by the temporary ligation of the optic nerve. Just before the induction of ischemia, the experimental eyes underwent intravitreal injection of amiloride. On day 7, the retinal damage in eyes that underwent amiloride treatment (and in those that did not undergo the treatment) was evaluated by histology and electroretinogram (ERG).

Results

Transient retinal ischemia caused retinal degeneration with thinning of the inner layer of the retina. The blockage of ASICs with amiloride significantly prevented retinal degeneration. ERG demonstrated that the reduction in a- and b-wave amplitudes induced by the transient retinal ischemia was significantly prevented by the application of amiloride.

Conclusions

The present study suggests that ASICs might, at least in part, play a pathophysiological role in ischemia-induced neurodegeneration. Blockage of ASICs may have a potential neuroprotective effect in ocular ischemic diseases.     

缺血预处理对大鼠视网膜缺血再灌注损伤保护作用

目的：探讨缺血预处理是否对视网膜缺血再灌注损伤有保护作用及其机理,方法：利用前房灌注生理盐水形成高眼压的视网膜缺血再灌注损伤的动物模型,视网膜缺血时间为1h分别于缺血前30min、24h或72h对大鼠一只眼5min短暂缺血即预处理,24h或72h后行视网膜电图（ERG）、电镜、光镜、丙二醛（MDA）及热休克蛋白70（HSP70）检测,或者一侧眼行5min假处理,24h后行1h缺血,24h或72h再行上述检测,所有对侧眼不作处理作对照,结果：与假处理相相比,缺血前24、72h进行预处理后的大鼠视网膜光镜、电镜表现损害明显减轻,ERGb波明显恢复（P＜0．01）,MDA含量降低（P＜0．01）,缺血前30min预处理的视网膜表现严重的损害,ERGb波几安全消失,结论：缺血预处理对视网膜缺血再灌注损伤有保护作用,且有一定时限性。     

Functional evaluation of retina and optic nerve in the rat model of chronic ocular hypertension

PURPOSE: To functionally characterize the rat retina and optic nerve after chronic elevation of the intraocular pressure (IOP) using electroretinography (ERG) and computerized pupillometry. METHODS: Chronic elevation of the IOP was induced in Brown Norway rats by combined injection of indocyanine green dye (ICG) into the anterior chamber and diode laser treatment, followed by ERG and pupil light reflex (PLR) monitoring. RESULTS: Laser treatment induced significant elevation of the IOP in operated eyes for 6 weeks, with maximal values observed 14 days postoperatively (ctrl=18.4+/-2.4 and operated=35+/-8.4 mmHg; mean+/-sd). Preoperative values for the PLR(ratio) were 68.5+/-4% (mean+/-sem; %). Three days postoperatively the PLR(ratio) decreased to 60.3+/-10.3%, but was not significantly different compared to preoperative values (p > 0.05 Kruskal-Wallis non-parametric test with Dunn's post-test). However, 7, 14 and 21 days postoperatively the PLR function dramatically decreased to 14.6+8.6, 11.5+/-6.7 and 12.6+/-4%, respectively, and was significantly smaller compared to preoperative values (p < 0.01). At day 28 the PLR significantly recovered and was not significantly different compared to preoperative values (PLR(ratio)=38.5+/-8.6, p > 0.05). However, 35 days after surgery the PLR started to decrease once again in the operated eyes (PLR(ratio)=17.2+/-7.4%) and was significantly smaller again compared to preoperative values (p < 0.05) The PLR values continued to decrease until the end of experiment (60 days postoperatively). ERG analysis of operated eyes revealed significantly decreased amplitudes of a- and b-waves 10d postoperatively, while oscillatory potentials (OPs) and flicker ERG (flERG) amplitudes were not detectable. However, 28 days postoperatively OPs significantly, but temporarily recovered, while a-wave, b-wave and flERG amplitudes did not significantly change compared to values observed 10d postoperatively. The ERG analysis of the operated eyes revealed significantly reduced amplitudes 60 days postoperatively. Histological analysis revealed degeneration of all retina layers and optic nerve axons. CONCLUSIONS: Chronic ocular hypertension in rats produces dramatic damage to all retinal layers and optic nerves observed by morphological and functional methods which significantly correlate with the IOP elevation. Outer retina of glaucomatous rats seems to be more susceptible to the damage due to chronic elevation of the IOP. Chronic hypertensive rat eyes have capacity to temporarily recover function of the inner retina and optic nerve.     

缺血后适应对视网膜缺血-再灌注损伤的保护作用

背景研究证明,缺血后适应（IPC）对多种组织器官的缺血缺氧损伤均有一定的抵抗作用,但其对视网膜缺血缺氧的作用仍受到关注。目的探讨IPC对大鼠视网膜缺血-再灌注损伤（RIRI）后视网膜结构和功能的保护作用。方法将36只健康雄性Wistar大鼠以随机数字表法分为正常对照组、伪手术组、缺血-再灌注组、IPC组。利用前房灌注生理盐水升高眼压至100mmHg（1mmHg=0．133kPa）维持60min的方法制备RIRI大鼠模型,实施IPC处理鼠亚分为再灌注后即刻、1min、10min组（即IPCⅠ组、IPCⅡ组、IPCⅢ组）,分别于实验后1d、7d行大鼠视网膜电图（ERG）检测,然后用过量麻醉法处死大鼠并制备视网膜切片,行苏木精-伊红染色,对各组大鼠视网膜厚度的变化和视网膜形态进行观察。采用SPSS13．0统计学软件的单因素方差分析对各组大鼠ERG各波振幅恢复率和视网膜厚度值的差异进行比较。结果实验后1d,与正常对照组大鼠比较,伪手术组大鼠视网膜结构接近正常,而缺血-再灌注组及IPCⅠ组、IPCⅡ组、IPCⅢ组大鼠视网膜均出现水肿,可见空泡变性,主要在内丛状层（IPL）及内核层（INL）。缺血-再灌注组及IPCⅠ组、IPCⅡ组、IPCⅢ组大鼠视网膜全层、INL、IPL及视网膜外层厚度值均明显高于正常对照组,差异均有统计学意义（均P〈0．05）。再灌注后7d,缺血-再灌注组大鼠视网膜全层厚度值明显低于正常对照组,差异均有统计学意义（均P〈0．05）,尤以INL、IPL显著。IPCⅠ组、IPCⅡ组、IPCⅢ组大鼠视网膜全层、INL、IPL及视网膜外层厚度值均明显高于缺血-再灌注组,差异均有统计学意义（均P〈0．05）。再灌注后7d,缺血-再灌注组、IPC各组大鼠ERG a波、b波和OPs振幅恢复率明显低于伪手术组和正常对照组大鼠,差异均有统计学意义（均P〈0．05）;而IPCⅠ组、IPCⅡ组、IPCⅢ组大鼠ERG a波、b波和OPs振幅恢复率明显高于缺血-再灌注组,差异均有统计学意义（均P〈0,05）。结论IPC对RIRI具有保护作用,在大鼠模型中,这种保护作用在再灌注后即刻至1min时最强。     

Glutamate transporter localization does not correspond to the temporary functional recovery and late degeneration after acute ocular ischemia in rats

PURPOSE: To determine whether the localization of retinal glutamate transporters is affected by retinal ischaemia and whether their ability to transport glutamate decreases with the progression of ischemic retinal and optic nerve degeneration. METHODS: Retinal ischemia was induced in rats by acutely increasing the intraocular pressure (IOP, 110 mmHg/60 min). Reperfusion was permitted for periods up to 60 days post-ischemia. Functional evaluation was performed by monitoring the pupil light reflexes (PLRs) and electroretinograms (flash, flicker ERG and oscillatory potentials). Glutamate transporter localization and D-aspartate (glutamate analogue) uptake were assessed by immunohistochemistry. RESULTS: Intense immunoreactivity for the retinal glutamate transporters (GLAST, GLT1, EAAC1 and EAAT5) was observed at all time points after the insult, despite severe retinal degeneration. D-aspartate was also normally accumulated in the ischemic retinas. Ten days post-operatively the PLR ratio (ratio=indirect/direct PLR=34+/-7.5%) was significantly less than the pre-operative value (pre-op=76.7+/-2.6%, p<0.05). However, 25 and 35 days post-operatively PLR ratios did not differ significantly from pre-operative values (44.4+/-6.9 and 53.8+/-9.6%, p>0.05). Forty-five and 60 days post-operatively the PLR ratio declined again and was significantly lower than the pre-operative value (33.8+8.7 and 26.2+8.9%, p<0.05). Statistical analysis revealed that all tested ERG components had significantly higher values at 32, but not at 42 and 58 days post-operatively when compared to the first time point recorded post-operatively (10 days). CONCLUSIONS: While retinal glutamate transport is compromised during an acute ischemic insult, consequent retinal recovery and degeneration are not due to a change in the excitatory amino acid transporter localization or D-aspartate (glutamate analogue) uptake. Rat retina and optic nerve are capable of spontaneous, but temporary, functional recovery after an acute ischemic insult.     

Vigabatrin effect on inner retinal function

OBJECTIVE: To determine the degree of electroretinal dysfunction in a group of patients taking Vigabatrin (VGB). Additionally, to investigate the role of cumulative dosage, the role of VGB alone or in combination with other anticonvulsants, and whether recent discontinuance of VGB affects electroretinal function as measured by the electroretinogram (ERG). DESIGN: Retrospective, comparative case series. PARTICIPANTS: Forty patients (18 male, 22 female) with a mean age of 35 years were studied as three groups: the VGB multitherapy group (n = 24) included those taking VGB with other anticonvulsants, the VGB monotherapy group (n = 9) included those taking VGB alone, and the off-VGB group (n = 7) included those who had discontinued VGB in the last 6 months. METHODS: Scotopic flash, photopic flash, and 30-Hz flicker ERG results were recorded according to the International Society for Clinical Electrophysiology of Vision (ISCEV) standard. The clinical electro-oculogram (EOG) results were recorded according to the ISCEV standard. MAIN OUTCOME MEASURES: Implicit time and amplitudes of the A- and B-waves of the flash and 30-Hz flicker ERGs were recorded. Summed amplitude of the first three oscillatory potential wavelets were recorded. The light-peak to-dark-trough Arden ratio of the EOG was evaluated. RESULTS: Although photopic ERG B-wave reduction was most frequent in patients in the VGB multitherapy group (48% of eyes), a significant number of eyes in all three groups had scotopic ERG B-wave reduction. The 30-Hz flicker ERG result was abnormally reduced in all three groups. There was no significant difference in the frequency of occurrence in ERG result abnormalities between the VGB monotherapy and VGB multitherapy groups. The EOG results revealed reduced Arden ratios in all three groups; however, there was a significantly lower frequency of EOG abnormalities noted in the off-VGB group (P = 0. 0373). There was no statistically significant relationship between the frequency of electrodiagnostic abnormalities and the duration of use or the total cumulative dosage of Vigabatrin in any of the three groups. CONCLUSIONS: These findings of scotopic ERG result abnormalities suggest that VGB alone has an effect on inner electroretinal function at the level of the Müller cell. Concomitant EOG abnormalities suggest a substantial effect of VGB on outer retinal function that may be reversible after cessation of VGB treatment.     

Origin of electroretinogram amplitude growth during light adaptation in pigmented rats

We assessed the growth of the rat photopic electroretinogram (ERG) during light adaptation and the mechanisms underlying this process. Full field ERG responses were recorded from anesthetized adult Brown-Norway rats at each minute for 20 min of light adaptation (backgrounds: 1.8, 2.1, 2.4 log scotopic cd m(-2)). The rat photopic b-wave amplitude increased with duration of light adaptation and its width at 33% maximal amplitude narrowed (by approximately 40 ms). These effects peaked 12-15 min after background onset. The narrowing of the b-wave reflected steepening of the b-wave recovery phase, with little change in the rising phase. OP amplitudes grew in proportion to the b-wave. Inhibition of inner retinal responses using TTX resulted in a greater relative growth of b-wave and OP amplitude compared with fellow control eyes, and delayed the change in recovery phase by approximately 5 min. Inhibition of all ionotropic glutamate receptors with CNQX/D-AP7 delayed both rising and recovery phases equally (approximately 12 ms) without altering b-wave width or the time course of adaptation changes. These outcomes suggest that inner retinal light responses are not directly responsible for b-wave amplitude growth, but may contribute to the change in its recovery phase during adaptation. A TTX-sensitive mechanism may help to hasten this process. The cone a-wave was isolated using PDA/L-AP4 or CNQX/L-AP4. A-wave amplitude (35 ms after stimulus onset) also increased with time during light adaptation and reached a maximum (130 +/- 29% above baseline) 12-15 min after background onset. B-wave amplitude growth in fellow control eyes closely followed the course and relative magnitude of cone a-wave amplitude growth. Hence, the increase of the cone response during light adaptation is sufficient to explain b-wave amplitude growth.     

眼球钝挫伤ERG与病理改变的关系

检查轻，重度兔眼挫伤后ＥＲＧａ，ｂ波及ＯＰｓ波的改变，用镧示踪法观察血视外屏障及其它组织结构改变。轻型挫伤ＥＲＧｂ波暂时降低，无示踪剂渗漏，光感受器外节轻度破坏。重型挫伤ＥＲＧａ，ｂ波及ＯＰｓ波明显降低，视风膜色素上皮细胞及外层视网膜细胞严得损害，伴有血视网膜外屏障破坏。结果提示眼球挫伤后视力的预后和组织损伤的程度有直接关系。     

Quantification of ischemic damage in the rat retina: a comparative study using evoked potentials, electroretinography, and histology

PURPOSE: To identify objective criteria to quantify visual function in the rat for developing therapeutic strategies to protect neuronal cells after ischemia. The impact of ocular ischemia on luminance and frequency-modulated contrast vision was compared with the function of outer retinal cells and the number of intact retinal ganglion cells (RGCs). METHOD: Ischemia was induced in Brown-Norway rats by elevating the intraocular pressure to 120 mm Hg for 30, 45, 60, and 90 minutes. Visual function was evaluated by visual evoked potentials (VEPs) in awake, freely moving rats. Retinal function was analyzed with scotopic and photopic electroretinography (ERG). RGCs were quantified in retinal flatmounts after postischemic injection of tracer into the superior colliculus. RESULTS: The response to flicker stimulation in VEP recordings decreased as the ischemic episodes increased. The susceptibility to ischemic damage was more pronounced when potentials were evoked with stimuli at higher frequencies. In ERG recordings, ischemia reduced oscillatory potentials and photopic flicker responses more intensely than scotopic a- and b-waves. In counting the RGCs, the reduced cell density correlated significantly with all electrophysiological parameters. The duration of ischemia with half-maximal inhibitory effect was between 36 and 58 minutes for VEPs and between 36 and 41 minutes for ERG, and it was 51 minutes for RGCs. CONCLUSIONS: The amounts of reduction in VEPs, ERG, and RGCs differed as the duration of ischemia increased. The electrophysiological parameters presented in this study may serve as a useful addition to morphologic evaluations in future neuroprotection studies in vivo.     

Steady-state electroretinograms and pattern electroretinograms in pigs

Background: Electroretinograms (ERG) or pattern-electroretinograms (PERG) could be valuable for the quantification of potential damage to the pig retina by experimental erbium:YAG laser treatment. We therefore performed a normative study of ERGs and PERGs in pigs. Methods: We recorded ERGs and PERGs under general anaesthesia in two experiments. In experiment 1 we examined eight eyes from six pigs of 20–25 kg body weight; in experiment 2 we examined four eyes from four pigs of 40–45 kg body weight. We used flash and checkerboard stimuli. In experiment 1, the stimulus parameters were mean luminance 48.3 cd/m² for checkerboard stimuli, 96.6 cd/m² for ERG, check sizes of 4°, 8°, and 16°, temporal frequencies were 16 Hz for ERG and 8 rev/s for PERG. Three measurements were repeated after two weeks. Stimulus parameters for experiment 2 were luminance 175 (350) cd/m², check sizes 1.6°, 3.2°, 6.7°, and 16°, temporal frequencies 6.3 Hz for ERG and 8 rev/s for PERG. Recordings were subjected to Fourier analysis. Results: In experiment 1 the mean ERG amplitude was 1.02±0.89 μV with a coefficient of variation of 42% for repeat sessions. The mean PERG amplitudes were 0.53±0.25 μV for 16° checks, 0.36±0.21 μV for 8°, and 0.25±0.17 μV for 4°. The mean coefficient of variation between two measurements was 103% for 16° checks, 24% for 8°, and 116% for 4°. In experiment 2 the mean ERG amplitude was 9.72±3.96 μV. The mean PERG amplitudes were 0.77±0.50 μV for 16° checks, 0.09±0.16 μV for 6.7°, 0.07±0.13 μV for 3.2°, and 0.08±0.09 μV for 1.6°. Conclusions: It was possible to record ERGs and PERGs in pigs. However, the ERG amplitudes were small; PERG amplitudes were even smaller in both groups and cannot be reliably recorded. A problem for both ERG and PERG was the high intra-individual and interindividual variability. Therefore, only very extensive damage to the retina by vitrectomy or Er:YAG laser treatment might lead to a significant change in the ERG or PERG amplitudes. Received: 6 April 2000 Revised: 6 June 2000 Accepted: 20 June 2000